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1
Howard-Quijano, Kimberly, Tatsuo Takamiya, Erica A. Dale, Jasmine Kipke, Yukiko Kubo, Tristan Grogan, Andyshea Afyouni, Kalyanam Shivkumar, and Aman Mahajan. "Spinal cord stimulation reduces ventricular arrhythmias during acute ischemia by attenuation of regional myocardial excitability." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 2 (August 1, 2017): H421—H431. http://dx.doi.org/10.1152/ajpheart.00129.2017.
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Myocardial ischemia creates autonomic nervous system imbalance and can trigger cardiac arrhythmias. We hypothesized that neuromodulation by spinal cord stimulation (SCS) will attenuate local cardiac sympathoexcitation from ischemia-induced increases in afferent signaling, reduce ventricular arrhythmias, and improve myocardial function during acute ischemia. Yorkshire pigs ( n = 20) were randomized to SCS (50 Hz at 200-μs duration, current 90% motor threshold) or sham operation (sham) for 30 min before ischemia. A four-pole SCS lead was placed percutaneously in the epidural space (T1–T4), and a 56-electrode mesh was placed over the heart for high-resolution electrophysiological recordings, including activation recovery intervals (ARIs), activation time, repolarization time, and dispersion of repolarization. Electrophysiological and hemodynamic measures were recorded at baseline, after SCS/sham, during acute ischemia (300-s coronary artery ligation), and throughout reperfusion. SCS 1) reduced sympathoexcitation-induced ARI and repolarization time shortening in the ischemic myocardium; 2) attenuated increases in the dispersion of repolarization; 3) reduced ventricular tachyarrythmias [nonsustained ventricular tachycardias: 24 events (3 sham animals) vs. 1 event (1 SCS animal), P < 0.001]; and 4) improved myocardial function (dP/d t from baseline to ischemia: 1,814 ± 213 to 1,596 ± 282 mmHg/s in sham vs. 1,422 ± 299 to 1,380 ± 299 mmHg/s in SCS, P < 0.01). There was no change in ventricular electrophysiology during baseline conditions without myocardial stress or in the nonischemic myocardium. In conclusion, in a porcine model of acute ventricular ischemia, SCS reduced regional myocardial sympathoexcitation, decreased ventricular arrhythmias, and improved myocardial function. SCS decreased sympathetic nerve activation locally in the ischemic myocardium with no effect observed in the normal myocardium, thus providing mechanistic insights into the antiarrhythmic and myocardial protective effects of SCS. NEW & NOTEWORTHY In a porcine model of ventricular ischemia, spinal cord stimulation decreased sympathetic nerve activation regionally in ischemic myocardium with no effect on normal myocardium, demonstrating that the antiarrhythmic effects of spinal cord stimulation are likely due to attenuation of local sympathoexcitation in the ischemic myocardium and not changes in global myocardial electrophysiology.
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Hoshida, S., T. Kuzuya, H. Fuji, N. Yamashita, H. Oe, M. Hori, K. Suzuki, N. Taniguchi, and M. Tada. "Sublethal ischemia alters myocardial antioxidant activity in canine heart." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 1 (January 1, 1993): H33—H39. http://dx.doi.org/10.1152/ajpheart.1993.264.1.h33.
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We examined antioxidant activity in the pre-conditioned canine myocardium with four 5-min episodes of regional ischemia and reperfusion. Immediately after repetitive brief ischemia, mitochondrial Mn-superoxide dismutase (SOD) activity in the ischemic myocardium significantly increased compared with that in the nonischemic myocardium (18.7 +/- 2.1 vs. 14.9 +/- 1.0 U/mg protein, P < 0.05). Although no difference was seen in the activity between these regions after 3 h of the sublethal ischemia, a significant increase in the activity of the ischemic myocardium reappeared after 24 h compared with that of the nonischemic myocardium (26.7 +/- 0.9 vs. 20.8 +/- 0.9 U/mg protein, P < 0.05). Mn-SOD content increased gradually in the ischemic myocardium after sublethal ischemia, with a peak after 24 h (2.8 +/- 0.1 vs. 2.1 +/- 0.1 microgram/mg protein, P < 0.05). There were no differences in the activity and content of Cu, Zn-SOD between these regions after sublethal ischemia. Activities of glutathione peroxidase and reductase were significantly higher and lower, respectively, in the ischemic myocardium than those of the nonischemic myocardium immediately after repetitive brief ischemia, but no differences between these regions were seen in activities after 3 or 24 h. These results indicate that a brief ischemic insult alters myocardial antioxidant activity not only immediately after but also 24 h after sublethal ischemia.
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Lee, C. Y., Amar Singh, Kevin J. Lee, Roy D. Goldfarb, and Min-Fu Tsan. "Correlation between myocardial glutathione content and extent of ischemia-reperfusion injury." Proceedings, annual meeting, Electron Microscopy Society of America 47 (August 6, 1989): 1068–69. http://dx.doi.org/10.1017/s0424820100157322.
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Considerable evidence suggests that myocardial injury may occur during reperfusion of the ischemic myocardium. Reactive oxygen species are generated during reperfusion which may play an important role in the genesis of myocardial reperfusion injury. Glutathione (GSH) is an important antioxidant in the heart. A decrease in myocardial GSH content has been observed during ischemia and reperfusion of the ischemic myocardiijm. We hypothesized that this depletion of GSH may be detrimental to the ability of the ischemic myocardium to protect itself against reactive oxygen species during reperfusion.In this study, anesthetized open chest pigs were subjected to coronary occlusion for 45 minutes and 2 hours reperfusion. Myocardial GSH was experimentally depleted by pretreatment with buthionine sulfoximine (BSO), a potent inhibitor of cellular GSH synthesis, and was augmented by intravenous administration of GSH. For ultrastructural study multiple subepicardial biopsies 3 mm deep were taken from myocardium supplied by the occluded artery. The biopsies were processed by routine procedures. Thin sections were stained with uranyl acetate and lead citrate and examined with a Philip EM 300 electron microscope.
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Spear, Joseph F., Subbuswamy K. Prabu, Domenico Galati, Haider Raza, Hindupur K. Anandatheerthavarada, and Narayan G. Avadhani. "β1-Adrenoreceptor activation contributes to ischemia-reperfusion damage as well as playing a role in ischemic preconditioning." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 5 (May 2007): H2459—H2466. http://dx.doi.org/10.1152/ajpheart.00459.2006.
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Protein kinase A (PKA) activation has been implicated in early-phase ischemic preconditioning. We recently found that during ischemia PKA activation causes inactivation of cytochrome- c oxidase (CcO) and contributes to myocardial damage due to ischemia-reperfusion. It may be that β-adrenergic stimulation during ischemia via endogenous catecholamine release activates PKA. Thus β-adrenergic stimulation may mediate both myocardial protection and damage during ischemia. The present studies were designed to determine the role of the β1-adrenergic receptor (β1-AR) in myocardial ischemic damage and ischemic preconditioning. Langendorff-perfused rabbit hearts underwent 30-min ischemia by anterior coronary artery ligation followed by 2-h reperfusion. Occlusion-reperfusion damage was evaluated by delineating the nonperfused volume of myocardium at risk and volume of myocardial necrosis after 2-h reperfusion. In some hearts ischemic preconditioning was accomplished by two 5-min episodes of global low-flow ischemia separated by 10 min before coronary occlusion-reperfusion. Orthogonal electrocardiograms were recorded, and coronary flow was monitored by a drip count. Three hearts from each experimental group were used to determine mitochondrial CcO and aconitase activities. Two-hour reperfusion after occlusion caused an additional decrease in CcO activity vs. that after 30-min occlusion alone. Blocking the β1-AR during occlusion-reperfusion reversed CcO activity depression and preserved myocardium at risk for necrosis. Similarly, mitochondrial aconitase activity exhibited a parallel response after occlusion-reperfusion as well as for the other interventions. Furthermore, classic ischemic preconditioning had no effect on CcO depression. However, blocking the β1-AR during preconditioning eliminated the cardioprotection. If the β1-AR was blocked after preconditioning, the myocardium was preserved. Interestingly, in both of the latter cases the depression in CcO activity was reversed. Thus the β1-AR plays a dual role in myocardial ischemic damage. Our findings may lead to therapeutic strategies for preserving myocardium at risk for infarction, especially in coronary reperfusion intervention.
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Thourani, Vinod H., Sukhdev S. Brar, Thomas P. Kennedy, Lisa R. Thornton, John A. Watts, Russell S. Ronson, Zhi-Qing Zhao, Anne L. Sturrock, John R. Hoidal, and Jakob Vinten-Johansen. "Nonanticoagulant heparin inhibits NF-κB activation and attenuates myocardial reperfusion injury." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 6 (June 1, 2000): H2084—H2093. http://dx.doi.org/10.1152/ajpheart.2000.278.6.h2084.
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Heparin reduces ischemia-reperfusion injury to myocardium. This effect has been attributed to complement inhibition, but heparin also has other activities that might diminish ischemia-reperfusion. To further probe these mechanisms, we compared heparin or an o-desulfated nonanticoagulant heparin with greatly reduced anticomplement activity. When given at the time of coronary artery reperfusion in a canine model of myocardial infarction, heparin or o-desulfated heparin equally reduced neutrophil adherence to ischemic-reperfused coronary artery endothelium, influx of neutrophils into ischemic-reperfused myocardium, myocardial necrosis, and release of creatine kinase into plasma. Heparin or o-desulfated heparin also prevented dysfunction of endothelial-dependent coronary relaxation following ischemic injury. In addition, heparin and o-desulfated heparin inhibited translocation of the transcription nuclear factor-κB (NF-κB) from the cytoplasm to the nucleus in human endothelial cells and decreased NF-κB DNA binding in human endothelium and ischemic-reperfused rat myocardium. Thus heparin and nonanticoagulant heparin decrease ischemia-reperfusion injury by disrupting multiple levels of the inflammatory cascade, including the novel observation that heparins inhibit activation of the proinflammatory transcription factor NF-κB.
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Wang, Chen-xi, Jun-jun Guo, An-jie Di, Yu Zhu, Wei-min Han, An-ran Cheng, Cheng Li, et al. "The Protective Effect of Cx43 Protein-Mediated Phosphocreatine on Myocardial Ischemia/Reperfusion Injury." Cardiology Research and Practice 2021 (January 22, 2021): 1–9. http://dx.doi.org/10.1155/2021/8838151.
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Objectives. To verify the protective effect of phosphocreatine on myocardium in an ischemic model and the possible mechanism of action. Methods. The model of myocardial ischemia/reperfusion (I/R) was established by the ligation balloon method. 30 SD rats were randomly divided into three groups, n = 10 in each group. Sham operation group: the coronary artery was not blocked and observed for 120 minutes. The ischemia/reperfusion (I/R) group was given ischemia for 30 minutes and ischemia reperfusion for 90 minutes. Phosphocreatine (PCr) group: after 30 minutes of ischemia, the rats were intraperitoneally injected with PCr (200 mg/kg) for 90 minutes. The animal groups of myocardial ischemia/reperfusion model in vitro were the same as those in vivo. The heart was removed by thoracotomy and washed immediately in H-K buffer solution. Then, the heart was installed on the Langendorff instrument. The concentration of PCr perfusion fluid in the PCr group was 10 mmol/L. The changes in coronary blood flow in isolated myocardium were recorded. The heart rate and electrocardiogram were recorded by RM6240BT. At the end of the experiment, myocardial pathological sections and Cx43 immunofluorescence staining were made, and the contents of malondialdehyde (MDA) in myocardial tissue were detected. Results. Phosphocreatinine treatment improved the myocardial ischemia model, performance in electrocardiogram (ECG) changes (ST segment apparent), and histological changes (decrease in necrotic myocardial cells, inflammatory cell infiltration, and a reduction in myocardial edema). At the same time, MDA decreased, while coronary blood flow and Cx43 expression significantly improved. Conclusions. Phosphocreatine can improve the electrocardiogram and restore histologic changes in ischemic myocardium and coronary blood flow. The postulated mechanism is by inhibiting the generation of free oxygen radicals and restoring the expression of Cx43 protein.
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A. Meenakshi, Martin, and Erik G. Seth. "Protective role of TAT-HSP70 after myocardial I/R injury." American Journal of BioMedicine 5, no. 3 (September 22, 2017): 279–84. http://dx.doi.org/10.18081/2333-5106/015-04/289-294.
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Myocardial ischemia reperfusion injury I/R adversely affects cardiac function. Heat shock proteins (HSPs) are a highly conserved family of proteins with diverse functions expressed by all cells exposed to environmental stress including myocardila injury. We investigated release of small constitutive heat shock proteins (HSPs) from mouse myocardium and the effects of TAT-HSP70 after myocardial I/R via occluding the left coronary artery (LAD). The results support the hypothesis that elevated HSPs in myocardium after ischemia and reperfusion and contributes to the inflammatory mechanism of myocardial functional injury. Further investigation of the significance of HSPs accumulation to the evolution of myocardial injury.
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Li, Kui, Chen Li, Ying Xiao, Tao Wang, and Y. James Kang. "Featured Article: The loss of copper is associated with the increase in copper metabolism MURR domain 1 in ischemic hearts of mice." Experimental Biology and Medicine 243, no. 9 (May 2018): 780–85. http://dx.doi.org/10.1177/1535370218773055.
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The distribution of copper (Cu) in the biological system is regulated by Cu transporters and chaperones. It has been known for a long time that myocardial ischemia is accompanied by the loss of Cu from the heart, but the mechanism by which this occurs remains unknown. The present study was undertaken to understand the relationship between Cu loss and alterations in Cu transporters during the pathogenesis of myocardial ischemia. Male mice (C57 BL/6J) were subjected to left anterior descending (LAD) coronary artery ligation to induce myocardial ischemia. Changes in Cu concentrations in serum and hearts were determined from blood and tissue samples harvested at different time points for a total of 28 days after the operation. Cu concentrations in the ischemic myocardium were continuously decreased starting at the fourth day after LAD artery ligation, gradually depleted by more than 80% of the normal level at the 10th day, and remained at the lowest level (about 20% of normal levels) thereafter. Serum Cu concentrations were correspondingly increased starting at the fourth day, reached to the highest level between day 7 and 10, and gradually recovered to the normal level until 21st day after the operation. Along with the same time course, the intracellular Cu exporter copper metabolism MURR domain 1 (COMMD1) was significantly and sustainably increased, but ATP7A and ATP7B were not significantly changed in the ischemic myocardium. These results suggest that during the pathogenesis of myocardial ischemia, COMMD1 would play a critical role in exporting Cu from the ischemic myocardium to the blood. Impact statement In this work, we found that copper efflux from the ischemic heart leads to the elevation of serum copper concentrations, addressing a long-term question related to serum copper elevation in myocardial ischemia patients. The efflux of copper from the ischemic heart results at least in part from the upregulation of copper metabolism MURR domain 1 (COMMD1) in the heart upon ischemic insult. This work provides a novel insight into copper homeostasis and alteration in cardiovascular system.
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Pan, Hui-Lin, Shao-Rui Chen, Gloria M. Scicli, and Oscar A. Carretero. "Cardiac interstitial bradykinin release during ischemia is enhanced by ischemic preconditioning." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 1 (July 1, 2000): H116—H121. http://dx.doi.org/10.1152/ajpheart.2000.279.1.h116.
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Ischemic preconditioning is known to protect the myocardium from ischemia-reperfusion injury. We examined the transmural release of bradykinin during myocardial ischemia and the influence of ischemic preconditioning on bradykinin release during subsequent myocardial ischemia. Myocardial ischemia was induced by occlusion of the left anterior descending coronary artery in anesthetized cats. Cardiac microdialysis was performed by implantation and perfusion of dialysis probes in the epicardium and endocardium. In eight animals, bradykinin release was greater in the endocardium than in the epicardium (14.4 ± 2.8 vs. 7.3 ± 1.7 ng/ml, P < 0.05) during 30 min of ischemia. In seven animals subjected to preconditioning, myocardial bradykinin release was potentiated significantly from 2.4 ± 0.6 ng/ml during the control period to 23.1 ± 2.5 ng/ml during 30 min of myocardial ischemia compared with the non-preconditioning group (from 2.7 ± 0.6 to 13.4 ± 1.9 ng/ml, P < 0.05, n = 6). Thus this study provides further evidence that transmural gradients of bradykinin are produced during ischemia. The results also suggest that ischemic preconditioning enhances bradykinin release in the myocardial interstitial fluid during subsequent ischemia, which is likely one of the mechanisms of cardioprotection of ischemic preconditioning.
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Stride, Nis, Steen Larsen, Martin Hey-Mogensen, Christina N. Hansen, Clara Prats, Daniel Steinbrüchel, Lars Køber, and Flemming Dela. "Impaired mitochondrial function in chronically ischemic human heart." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 11 (June 1, 2013): H1407—H1414. http://dx.doi.org/10.1152/ajpheart.00991.2012.
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Chronic ischemic heart disease is associated with myocardial hypoperfusion. The resulting hypoxia potentially inflicts damage upon the mitochondria, leading to a compromised energetic state. Furthermore, ischemic damage may cause excessive production of reactive oxygen species (ROS), producing mitochondrial damage, hereby reinforcing a vicious circle. Ischemic preconditioning has been proven protective in acute ischemia, but the subject of chronic ischemic preconditioning has not been explored in humans. We hypothesized that mitochondrial respiratory capacity would be diminished in chronic ischemic regions of human myocardium but that these mitochondria would be more resistant to ex vivo ischemia and, second, that ROS generation would be higher in ischemic myocardium. The aim of this study was to test mitochondrial respiratory capacity during hyperoxia and hypoxia, to investigate ROS production, and finally to assess myocardial antioxidant levels. Mitochondrial respiration in biopsies from ischemic and nonischemic regions from the left ventricle of the same heart was compared in nine human subjects. Maximal oxidative phosphorylation capacity in fresh muscle fibers was lower in ischemic compared with nonischemic myocardium ( P < 0.05), but the degree of coupling (respiratory control ratio) did not differ ( P > 0.05). The presence of ex vivo hypoxia did not reveal any chronic ischemic preconditioning of the ischemic myocardial regions ( P > 0.05). ROS production was higher in ischemic myocardium ( P < 0.05), and the levels of antioxidant protein expression was lower. Diminished mitochondrial respiration capacity and excessive ROS production demonstrate an impaired mitochondrial function in ischemic human heart muscle. No chronic ischemic preconditioning effect was found.
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Bosnjak, Zeljko J., and Zhi-Dong Ge. "The application of remote ischemic conditioning in cardiac surgery." F1000Research 6 (June 16, 2017): 928. http://dx.doi.org/10.12688/f1000research.11018.1.
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Perioperative myocardial ischemia and infarction are the leading causes of morbidity and mortality following anesthesia and surgery. The discovery of endogenous cardioprotective mechanisms has led to testing of new methods to protect the human heart. These approaches have included ischemic pre-conditioning, per-conditioning, post-conditioning, and remote conditioning of the myocardium. Pre-conditioning and per-conditioning include brief and repetitive periods of sub-lethal ischemia before and during prolonged ischemia, respectively; and post-conditioning is applied at the onset of reperfusion. Remote ischemic conditioning involves transient, repetitive, non-lethal ischemia and reperfusion in one organ or tissue (remote from the heart) that renders myocardium more resistant to lethal ischemia/reperfusion injury. In healthy, young hearts, many conditioning maneuvers can significantly increase the resistance of the heart against ischemia/reperfusion injury. The large multicenter clinical trials with ischemic remote conditioning have not been proven successful in cardiac surgery thus far. The lack of clinical success is due to underlying risk factors that interfere with remote ischemic conditioning and the use of cardioprotective agents that have activated the endogenous cardioprotective mechanisms prior to remote ischemic conditioning. Future preclinical research using remote ischemic conditioning will need to be conducted using comorbid models.
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Hsu, Edward W., Rong Xue, Alex Holmes, and John R. Forder. "Delayed reduction of tissue water diffusion after myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 2 (August 1, 1998): H697—H702. http://dx.doi.org/10.1152/ajpheart.1998.275.2.h697.
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The apparent diffusion coefficient (ADC) of water after regional myocardial ischemia was measured in isolated, perfused rabbit hearts by using magnetic resonance imaging (MRI) techniques. After ligation of the left anterior descending coronary artery, the ADC of the nonperfused region showed a gradual but significant decreasing trend over time, whereas that of the normally perfused myocardium remained constant. Morphological analysis revealed that the ADC decrease reflected the expansion of a subregion of reduced ADC within the nonperfused myocardium. The dynamics of the diffusion change and the morphological progression of the affected tissue suggest that the ADC decrease may be linked to the onset of myocardial infarction, which is known to involve myocyte swelling. The ADC reduction provides a potentially valuable MRI tissue-contrast mechanism for noninvasively determining the viability of the ischemic myocardium and assessing the dynamics of acute myocardial infarction.
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Lin, Jijin, Yuguang Li, Shuguang Lin, Qing Liang, and Xuerui Tan. "The effect of delayed preconditioning on connexin 43 in ischemic myocardiumThis paper is one of a selection of papers in this Special Issue, entitled International Symposium on Recent Advances in Molecular, Clinical, and Social Medicine, and has undergone the Journal's usual peer-review process." Biochemistry and Cell Biology 85, no. 2 (April 2007): 175–81. http://dx.doi.org/10.1139/o07-003.
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The objective of this study is to investigate the effects of preconditioning on the restoration and distribution of connexin 43 (Cx43) in ischemic myocardium in dogs. In this study, 40 dogs were randomly divided into 5 groups of 8 as follows: control, 0hI-R (ischemia followed by 0 h reperfusion), 6hI-R (ischemia followed by 6 h reperfusion), 24hI-R (ischemia followed by 24 h reperfusion), and 48hI-R (ischemia followed by 48 h reperfusion). Four dogs in each group were preconditioned with brief episodes of ischemia prior to the respective treatments and were referred as the PC groups, while the other 4 were not preconditioned and were referred as the nonPC groups. The myocardial ischemia was induced by ligation of the left anterior descending coronary artery. The expression and distribution of Cx43 within the ischemic myocardium were measured by Western blot analysis and studied using laser confocal microscopy using a double-label immunohistochemistry technique. Compared with the control group, there was a significant reduction in Cx43 content within ischemic myocardium of all test groups both with and without PC (P < 0.01, P < 0.05). Within the 0hI-R, 6hI-R, and 24hI-R groups, an insignificant difference was found in the expression and distribution of Cx43 within the ischemic region between the PC and the nonPC groups. However, in the 48hI-R group, the area and intensity of Cx43 staining within the ischemic region of the PC dogs were significantly larger and more intense than those of the nonPC dogs (P < 0.01), and the ratio of Cx43 pixel density in intercalated disk areas to that in side-to-side junction areas in the PC dogs was significantly greater than that in nonPC dogs (P < 0.01). Our results suggest that preconditioning has a significant effect on the restoration and distribution of Cx43 in the ischemic myocardium in dogs after 48 h. Hence, preconditioning may be a plausible cause for the observed reductions in cardiac arrhythmias.
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Dauber, I. M., E. J. Lesnefsky, K. M. VanBenthuysen, J. V. Weil, and L. D. Horwitz. "Reactive oxygen metabolite scavengers decrease functional coronary microvascular injury due to ischemia-reperfusion." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 1 (January 1, 1991): H42—H49. http://dx.doi.org/10.1152/ajpheart.1991.260.1.h42.
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The role of reactive oxygen metabolites in ischemia-reperfusion coronary microvascular injury is unclear. To investigate this problem, we tested the effects of the reactive oxygen metabolite scavengers superoxide dismutase (SOD) and dimethylthiourea (DMTU) on ischemia-reperfusion-induced coronary microvascular dysfunction. As an index of vascular function, we assessed microvascular permeability with a double radioisotope protein leak index (PLI) method. Anesthetized dogs underwent 60 min of ischemia via left anterior descending (LAD) occlusion followed by 60 min of reperfusion. Untreated animals (n = 7) received saline. SOD-treated animals (n = 6) received 140 U.kg-1.min-1 (6.6 mg.kg-1.min-1) bovine SOD throughout ischemia and reperfusion. DMTU-treated animals (n = 5) received a 500 mg/kg bolus 30 min before ischemia. At the beginning of reperfusion, radiolabeled autologous protein (113mIn transferrin) and red blood cells (99mTc) were given intravenously for the assessment of permeability. In untreated dogs, ischemia-reperfusion increased the PLI of ischemic (flow less than 20 ml.min-1.100 g-1) myocardium more than threefold compared with that of nonischemic (flow greater than 100 ml.min-1.100 g-1) myocardium (ischemic-to-nonischemic PLI ratio = 3.49 +/- 0.48). SOD reduced the PLI of ischemic myocardium by 45% and DMTU reduced it by 66% (PLI = 9.25 +/- 1.30, 5.04 +/- 1.18, and 3.16 +/- 0.94, untreated, SOD, and DMTU, respectively). The PLI was increased proportional to the regional severity of ischemic blood flow. Both SOD and DMTU reduced the increase in protein leak at all levels of regional ischemic blood flow. Neither SOD nor DMTU increased regional myocardial blood flow to the occluded LAD zone.(ABSTRACT TRUNCATED AT 250 WORDS)
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Li, Chuanfu, Race L. Kao, Tuanzhu Ha, Jim Kelley, I. William Browder, and David L. Williams. "Early activation of IKKβ during in vivo myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 3 (March 1, 2001): H1264—H1271. http://dx.doi.org/10.1152/ajpheart.2001.280.3.h1264.
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We have demonstrated that in vitro brief ischemia activates nuclear factor (NF)-κB in rat myocardium. We report in vivo ischemia-reperfusion (I/R)-induced NF-κB activation, IκB kinase -β (IKKβ) activity, and IκBα phosphorylation and degradation in rat myocardium. Rat hearts were subjected to occlusion of the coronary artery for up to 45 min or occlusion for 15 min followed by reperfusion for up to 3 h. Cytoplasmic and nuclear proteins were isolated from ischemic and nonischemic areas of each heart. NF-κB activation was increased in the ischemic area (680%) after 10 min of ischemia and in the nonischemic area (350%) after 15 min of ischemia and remained elevated during prolonged ischemia and reperfusion. IKKβ activity was markedly increased in ischemic (1,800%) and nonischemic (860%) areas, and phosphorylated IκBα levels were significantly elevated in ischemic (180%) and nonischemic (280%) areas at 5 min of ischemia and further increased after reperfusion. IκBα levels were decreased in the ischemic (45%) and nonischemic (36%) areas after 10 min of ischemia and remained low in the ischemic area during prolonged ischemia and reperfusion. The results suggest that in vivo I/R rapidly induces IKKβ activity and increases IκBα phosphorylation and degradation, resulting in NF-κB activation in the myocardium.
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Tani, M., H. Hasegawa, Y. Suganuma, K. Shinmura, Y. Kayashi, and Y. Nakamura. "Protection of ischemic myocardium by inhibition of contracture in isolated rat heart." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 6 (December 1, 1996): H2515—H2519. http://dx.doi.org/10.1152/ajpheart.1996.271.6.h2515.
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Protection of the ischemic myocardium by pretreatment with a high dose of 2,3-butanedione monoxime (BDM) is attributed to the enhancement of glycolytic ATP production rather than to the inhibition of contracture during mild ischemia. Our objective was to investigate whether the inhibition of contracture would protect the arrested heart during prolonged ischemia. Isolated perfused rat hearts were subjected to 30 min of low-flow ischemia followed by reperfusion. Ischemic hearts were treated with BDM (5 mmol/l) after beating stopped. BDM ameliorated the increase in intraventricular pressure after ischemia without significant changes in ATP levels and with a decreased accumulation of lactate. BDM treatment accelerated the recovery of function and high-energy phosphates with reduced myocardial Ca2+ overload. The results of this study suggested that inhibition of contracture can protect the heart from ischemia-reperfusion injury.
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Cinca, J., A. Bardaji, J. Figueras, A. Salas-Caudevilla, A. Serrano, and J. Rius. "Effects of regional denervation on epicardial DC electrograms during coronary occlusion in pigs." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 1 (July 1, 1987): H138—H146. http://dx.doi.org/10.1152/ajpheart.1987.253.1.h138.
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Sympathetic innervation of the normal and acutely ischemic myocardium and the effects of regional myocardial sympathetic denervation of the ischemic area on the evolving electrical changes during coronary occlusion were assessed in pigs anesthetized with pentobarbital sodium. The histofluorescence of the adrenergic nerve fibers (glyoxylic acid reaction), which in the normal myocardium were distributed in a diffuse network, decreased slightly after 45 min of occlusion of the left anterior descending (LAD) coronary artery and nearly disappeared after 2 h of ischemia. Topical application of phenol (carbolic acid, 88%) to the coronary arterial wall produced a transmural loss of catecholamine histofluorescence in the distal myocardium supplied by the phenol-treated arterial segment. Mapping of the epicardial direct current (DC) electrograms in sympathetically denervated and in nondenervated sections of the same ischemic area, using three rows of seven cotton-wick electrodes, was performed in eight pigs and validated in eight other nondenervated pigs. During 45 min of LAD occlusion, the denervated area, with respect to the nondenervated region, showed a greater decline in T-Q segment depression after 20 min of ischemia (P less than 0.0001), a lesser degree of S-T segment elevation throughout the study (P less than 0.0001), a delayed development of monophasic potentials (P less than 0.05), a minor degree of S-T segment alternans (P less than 0.0001), and a less marked, but still present, period of transient electrical recovery. Thus acute regional myocardial sympathectomy reduces the magnitude of the local electrical manifestations of acute myocardial ischemia in the in situ pig heart. Also in this model, sympathetic fibers appeared to lose the catecholamine histofluorescence after 2 h of acute ischemia.
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Liu, Ai-Hua, Yi-Min Bao, Xing-Yu Wang, and Zhi-Xiong Zhang. "Cardio-Protection by Ginkgo biloba Extract 50 in Rats with Acute Myocardial Infarction is Related to Na+–Ca2+ Exchanger." American Journal of Chinese Medicine 41, no. 04 (January 2013): 789–800. http://dx.doi.org/10.1142/s0192415x13500535.
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Ginkgo biloba has been used for medical purposes for centuries in traditional Chinese medicine. Ginkgo biloba extract 50 (GBE50) is a new standardized GBE product that matches the standardized German product as EGb761. This paper is aimed at studying the cardio-protection effects of GBE50 Salvia miltiorrhiza on myocardial function, area at risk, myocardial ultra-structure, and expression of calcium handling proteins in rat ischemic myocardium. Myocardium ischemia was induced by the left anterior descending (LAD) coronary artery occlusion and myocardial function was recorded by a transducer advanced into the left ventricle on a computer system. In vitro myocardial infarction was measured by 2,3,5-triphenyltetrazolium chloride (TTC) and Evans blue staining of heart sections. Morphological change was evaluated by electric microscopy and Western blotting was used for protein expression. Hemodynamic experiments in vivo showed that postischemic cardiac contractile function was reduced in ischemic rats. Salvia miltiorrhiza (7.5 g/kg/d×7) and Ginkgo biloba extract 50 (GBE50) (100 mg/kg/d×7) improved post-schemic cardiac diastolic dysfunction while not affecting the systolic function. In hearts of GBE50 group and Salvia miltiorrhiza (SM) group, the area at risk was significantly reduced and myocardial structure was better-preserved. Moreover, Na +– Ca 2+ exchanger (NCX) expression increase and sarcoplasmic reticulum Ca 2+– ATPase 2 (SERCA2), LTCC, and ryanodine receptor 2 (RyR2) expression decreases were smaller than those in ischemia group. There was a significant difference between the GBE50 and ischemia group in NCX expression. GBE50 could improve recovery in contractile function and prevent myocardium from ischemia damage, which may be caused by attenuating the abnormal expression of NCX.
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Abdrahmanova, A. I., N. B. Amirov, and N. A. Cibulkin. "Application of Perfusion Single Photon Emission Computed Tomography of the Myocardium in Pain-Free Myocardial Ischemia." Russian Archives of Internal Medicine 10, no. 5 (October 9, 2020): 340–47. http://dx.doi.org/10.20514/2226-6704-2020-10-5-340-347.
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This literature review provides data on the use of single-photon emission computed tomography of myocardium in silent myocardial ischemia. The presence of silent myocardial ischemia increases the risk of cardiovascular complications several times and may be the first manifestation of coronary heart disease. Assessing the state of morphofunctional processes in the myocardium is the main goal of diagnostic imaging using singlephoton emission computed tomography of the myocardium. This allows to get three-dimensional image of left ventricle with information about distribution of perfusion volume across myocardium, makes it possible to more accurately differentiate such condition as silent myocardial ischemia. Conducting single-photon emission computed tomography in ECG synchronization mode allows you to visualize the kinetics of the myocardial walls in different phases of the cardiac cycle and thereby simultaneously assess the functional state of the left ventricular myocardium. Indicators of contractile function of the left ventricular myocardium in areas of transient hypoperfusion can be predictors of cardiac events after myocardial infarction and independent predictors of perioperative cardiac events in patients undergoing cardiac surgery. Performing single-photon emission computed tomography in ECG-synchronization mode allows visualizing kinetics of myocardial walls in different phases of cardiac cycle and thereby simultaneously assessing functional state of left ventricle myocardium. In combination with physical exercise and pharmacological tests, it helps to identify coronary stenosis among patients with silent myocardial ischemia. Perfusion single-photon emission computed tomography of myocardium is a necessary tool for stratification and assessment of prognosis of cardiac diseases in asymptomatic patients.
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Cha, Jehyun, Joonghyun Ryu, Jin-Ho Choi, and Deok-Soo Kim. "Medial-ABC: an algorithm for the correspondence between myocardium and coronary artery mesh models based on the medial axis of coronary artery." Journal of Computational Design and Engineering 7, no. 6 (August 6, 2020): 736–60. http://dx.doi.org/10.1093/jcde/qwaa054.
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Abstract The role of coronary arteries is to supply sufficient blood to myocardium. Obstruction of coronary arteries limits blood supply and causes myocardial ischemia or acute myocardial infarction, a major cause of human death. Hence, the quantification of the regional amount of heart muscle subtended by obstructed coronary arteries is of critical value in clinical medicine. However, conventional methods are inaccurate and frequently disagree with clinical practice. This study proposes a novel medial-axis-based correspondence (Medial-ABC) algorithm to find the correspondence between myocardium and coronary artery in order to segment regional myocardium at risk subtended by any potentially obstructed coronary artery. Given the triangular mesh models of coronary artery and myocardium, the proposed algorithm (i) computes the medial axis of coronary artery, (ii) finds the correspondence using the medial axis of coronary artery, and (iii) segments the coronary artery and myocardium. The proposed algorithm provides a robust mathematical linkage between myocardium at risk and supplying coronary arteries so that ischemic myocardial regions can be accurately identified. Hence, both the extent and severity of myocardial ischemia can be quantified effectively, efficiently, and accurately. Furthermore, the constructed mesh model of segmented coronary artery and myocardium can be post-processed for applications such as building optimization models of cardiac systems. The CardiacVis program, which implements the Medial-ABC algorithm, is freely available at Voronoi Diagram Research Center (http://voronoi.hanyang.ac.kr/software/cardiacvis) and will be an invaluable tool for quantitative patient-specific risk stratification in clinical practice.
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De Meyer, Simon F., Alexander S. Savchenko, Michael S. Haas, Daphne Schatzberg, Michael C. Carroll, Alexandra Schiviz, Barbara Dietrich, Hanspeter Rottensteiner, Friedrich Scheiflinger, and Denisa D. Wagner. "Protective anti-inflammatory effect of ADAMTS13 on myocardial ischemia/reperfusion injury in mice." Blood 120, no. 26 (December 20, 2012): 5217–23. http://dx.doi.org/10.1182/blood-2012-06-439935.
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Abstract Coronary heart disease is a major cause of death in the western world. Although essential for successful recovery, reperfusion of ischemic myocardium is inevitably associated with reperfusion injury. To investigate a potential protective role of ADAMTS13, a protease cleaving von Willebrand factor multimers, during myocardial ischemia/reperfusion, we used a mouse model of acute myocardial infarction. We found that Adamts13−/− mice developed larger myocardial infarctions than wild-type control mice, whereas treatment of wild-type mice with recombinant human ADAMTS13 (rhADAMTS13) led to smaller infarctions. The protective effect of ADAMTS13 was further confirmed by a significant reduction of cardiac troponin-I release and less myocardial apoptosis in mice that received rhADAMTS13 compared with controls. Platelets adherent to the blood vessel wall were observed in few areas in the heart samples from mice treated with vehicle and were not detected in samples from mice treated with rhADAMTS13. However, we observed a 9-fold reduction in number of neutrophils infiltrating ischemic myocardium in mice that were treated with rhADAMTS13, suggesting a potent anti-inflammatory effect of ADAMTS13 during heart injury. Our data show that ADAMTS13 reduces myocardial ischemia/reperfusion injury in mice and indicate that rhADAMTS13 could be of therapeutic value to limit myocardial ischemia/reperfusion injury.
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Caswell, John E., Micah B. Strange, David M. Rimmer, Michael F. Gibson, Phillip Cole, and David J. Lefer. "A novel hemoglobin-based blood substitute protects against myocardial reperfusion injury." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 4 (April 2005): H1796—H1801. http://dx.doi.org/10.1152/ajpheart.00905.2004.
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HBOC-201 (Biopure; Cambridge, MA) is a glutaraldehyde-polymerized bovine hemoglobin (Hb) solution that is stroma free, has lower viscosity than blood, and promotes O2unloading. We investigated the effects of HBOC-201 in a canine model of myocardial ischemia-reperfusion injury. Dogs were anesthetized and subjected to 90 min of regional myocardial ischemia and 270 min of reperfusion. HBOC-201 or 0.9% saline vehicle equivalent to 10% total blood volume was infused 30 min before myocardial ischemia. Hemodynamic data and peripheral blood samples were taken at baseline, 1 h of myocardial ischemia, and 1, 2, and 4 h of reperfusion. At 270 min of reperfusion, the area at risk (AAR) per left ventricle and the area of infarction (Inf) per AAR were determined. The myocardial AARs in the two study groups were similar. In addition, myocardial blood flow (as measured by radioactive microspheres) in the ischemic zone was similar between the vehicle and HBOC-201 groups. HBOC-201-infused dogs demonstrated a significant ( P < 0.01) 56% reduction in Inf/AAR. Analysis of blood samples taken at 4 h of reperfusion showed a significant ( P < 0.05) reduction in creatine kinase MB isoform for the HBOC-201 group. Histological analysis of the myocardium demonstrated significant ( P < 0.01) reductions in neutrophil infiltration in the HBOC-201 group. These data indicate that treatment with HBOC-201 before myocardial ischemia-reperfusion reduces the extent of myocardial inflammation and ischemia-reperfusion injury in the canine myocardium.
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Osborne, J. A., and A. M. Lefer. "Cardioprotective actions of thromboxane receptor antagonism in ischemic atherosclerotic rabbits." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 2 (August 1, 1988): H318—H324. http://dx.doi.org/10.1152/ajpheart.1988.255.2.h318.
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Atherosclerosis was induced in New Zealand White rabbits by feeding them a 0.5% cholesterol-enriched rabbit chow for 10–12 wk. Half of the cholesterol-fed rabbits were given BM 13505, a specific thromboxane A2/endoperoxide (TxA2/PGH2) receptor antagonist, and the other half were given its vehicle (i.e., 2% Na2CO3). At the end of 10–12 wk, the rabbits underwent experimental myocardial ischemia or an identical sham operation, except that the coronary artery was not occluded. BM 13505 was shown to protect the ischemic rabbit myocardium by three different methods: 1) maintenance of myocardial tissue creatine kinase (CK) activity in the ischemic myocardium; 2) reduced loss of free amino nitrogen-containing compounds from the myocardium; and 3) blunting the rise of plasma CK activity. Part of the mechanism for these effects may be due to inhibition of platelet aggregation and blockade of the vasoconstrictor effect of TxA2. However, these protective effects were not due to differences in myocardial oxygen demand among the groups. Finally, BM 13505 exhibited an antiatherogenic effect by reducing the deposition of cholesterol in the aortic wall and by retarding plaque formation in coronary arteries. However, it does not achieve this antiatherogenic effect by lowering plasma cholesterol concentrations or by scavenging superoxide free radicals. Thus blockade of TxA2 receptors exerts a variety of beneficial effects that reduce the severity of ischemic damage resulting from myocardial ischemia.
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Vinten-Johansen, Jakob, Zhi-Qing Zhao, Rong Jiang, Amanda J. Zatta, and Geoffrey P. Dobson. "Preconditioning and postconditioning: innate cardioprotection from ischemia-reperfusion injury." Journal of Applied Physiology 103, no. 4 (October 2007): 1441–48. http://dx.doi.org/10.1152/japplphysiol.00642.2007.
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Reperfusion is the definitive treatment to salvage ischemic myocardium from infarction. A primary determinant of infarct size is the duration of ischemia. In myocardium that has not been irreversibly injured by ischemia, reperfusion induces additional injury in the area at risk. The heart has potent innate cardioprotective mechanisms against ischemia-reperfusion that reduce infarct size and other presentations of postischemic injury. Ischemic preconditioning (IPC) applied before the prolonged ischemia exerts the most potent protection observed among known strategies. It has been assumed that IPC exerts protection during ischemia. However, recent data suggest that cardioprotection is also exerted during reperfusion. Postconditioning (PoC), defined as brief intermittent cycles of ischemia alternating with reperfusion applied after the ischemic event, has been shown to reduce infarct size, in some cases equivalent to that observed with IPC. Although there are similarities in mechanisms of cardioprotection by these two interventions, there are key differences that go beyond simply exerting these mechanisms before or after ischemia. A significant limitation of IPC has been the inability to apply this maneuver clinically except in situations where the ischemic event can be predicted. On the other hand, PoC is applied at the point of service in the hospital (cath-lab for percutaneous coronary intervention, coronary artery bypass grafting, and other cardiac surgery) where and when reperfusion is initiated. Initial clinical studies are in agreement with the success and extent to which PoC reduces infarct size and myocardial injury, even in the presence of multiple comorbidities.
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Hori, M., J. Tamai, M. Kitakaze, K. Iwakura, K. Gotoh, K. Iwai, Y. Koretsune, T. Kagiya, A. Kitabatake, and T. Kamada. "Adenosine-induced hyperemia attenuates myocardial ischemia in coronary microembolization in dogs." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 1 (July 1, 1989): H244—H251. http://dx.doi.org/10.1152/ajpheart.1989.257.1.h244.
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We have recently reported that coronary microembolization sustains myocardial ischemia with hyperemic response of coronary blood flow (CBF) induced by massive release of adenosine from the ischemic myocardium. In this study, we tested the hypothesis that this hyperemic flow caused by released adenosine improves myocardial ischemia. In eight dogs (control), microspheres (5.0 X 10(4)/ml of base-line CBF) were repetitively injected until CBF decreased toward zero, and the changes in CBF, fractional shortening, lactate extraction ratio (LER), and adenosine release were studied. In 15 other dogs, an identical procedure was done with an intracoronary infusion of prazosin (4 micrograms.kg-1.min-1, n = 8) or theophylline (0.1 mg.kg-1.min, n = 7) to elucidate the effect of adenosine, since prazosin inhibits release of adenosine from ischemic myocardium and theophylline blocks adenosine receptors. In 16 other dogs, hemodynamic and metabolic parameters were examined with and without these drugs after a single injection of microspheres (1.0 X 10(5)/ml of base-line CBF). In the control group, CBF increased to 170 +/- (SE) 14% of the base-line CBF at 16-30% of maximal embolization. In contrast, intracoronary infusion of prazosin markedly attenuated adenosine release and hyperemic response and significantly deteriorated both fractional shortening and LER. Theophylline also significantly attenuated the hyperemic response and tended to decrease both fractional shortening and LER. A salutary effect of adenosine release was further confirmed by the improvement of ischemic changes in the same dog after withdrawal of prazosin and theophylline associated with an increase in CBF. Thus we conclude that adenosine released from ischemic myocardium improves ischemia in microembolization through the hyperemic response.
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Brown, TA. "Hibernating myocardium." American Journal of Critical Care 10, no. 2 (March 1, 2001): 84–91. http://dx.doi.org/10.4037/ajcc2001.10.2.84.
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According to estimates, up to 50% of patients with coronary artery disease and impaired left ventricular function have areas of viable myocardium. This dysfunctional, yet viable myocardial tissue, which can improve functionally after myocardial oxygen supply is reestablished, has been called hibernating myocardium. The possible pathophysiological mechanism that leads to hibernating myocardium is controversial: is the phenomenon due to persistent ischemia or is it the result of repetitive episodes of ischemia and reperfusion, such as myocardial stunning? Regardless of the mechanism, the presence of viable myocardial tissue indicates that structural and biochemical cellular changes occur, and the recovery of left ventricular function after revascularization depends on the severity and extent of these changes. Whether these changes reflect a long-lasting state of cellular dedifferentiation, an adaptive process that is reversible, or eventually lead to cellular degeneration has not been determined. Perhaps early detection of hibernating myocardial tissue via noninvasive imaging techniques used to assess contractile response, integrity of the cellular membrane, myocardial metabolism, and myocardial blood flow and subsequent early coronary revascularization may prevent infarction and deterioration in left ventricular function. Knowledge that reversible changes and areas of viable myocardium can occur in patients with left ventricular dysfunction will assist healthcare providers in the care and management of patients with hibernating myocardium.
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Becker, Lewis C., Richmond W. Jeremy, Jutta Schaper, and Wolfgang Schaper. "Ultrastructural assessment of myocardial necrosis occurring during ischemia and 3-h reperfusion in the dog." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 1 (July 1, 1999): H243—H252. http://dx.doi.org/10.1152/ajpheart.1999.277.1.h243.
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To determine whether myocardial necrosis may occur during postischemic reperfusion, electron microscopy was used to identify morphological features of irreversible injury in myocardial samples taken from anesthetized dogs with 90-min ischemia and 0-, 5-, 90-, or 180-min reperfusion. In samples without detectable collateral blood flow, necrosis was almost complete, whether or not the myocardium was reperfused. In samples with collateral flow, necrosis was more frequent after 180-min reperfusion than in the absence of reperfusion, despite similar collateral flows in the two groups. Excess of necrosis after 180-min reperfusion was evident in endocardium (ischemia only: 4 of 13, 180-min reflow: 14 of 20; P = 0.03) and midwall (ischemia only: 9 of 25, 180-min reflow: 29 of 45; P = 0.02). Multiple logistic regression with variables of collateral flow and transmural position was used to determine risk of irreversible injury in 111 samples from ischemic myocardium without reperfusion (model predictive accuracy = 75%, P < 0.00001) and to predict risk of necrosis in myocardium reperfused for 180 min. Of 65 samples from endocardium and midwall with detectable collateral flow, the model predicted necrosis in 23 samples but necrosis was observed in 43 samples ( P < 0.01). Reperfusion duration was a determinant of frequency of irreversible injury. Multiple logistic regression for 186 samples from myocardium reperfused for 5, 90, or 180 min showed that reperfusion duration was an independent predictor of irreversible injury ( P = 0.0003) when collateral flow and transmural location were accounted for. These findings are consistent with the occurrence of necrosis during reperfusion in myocardium exposed to substantial, prolonged ischemia but with sufficient residual perfusion to avoid necrosis during the period of flow impairment.
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Engler, R. L., M. D. Dahlgren, M. A. Peterson, A. Dobbs, and G. W. Schmid-Schonbein. "Accumulation of polymorphonuclear leukocytes during 3-h experimental myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 1 (July 1, 1986): H93—H100. http://dx.doi.org/10.1152/ajpheart.1986.251.1.h93.
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Recent evidence indicates that mechanical obstruction of capillaries by leukocytes plays an important role in the "no-reflow" phenomenon in the heart. This entrapment of leukocytes in the microcirculation precedes their recognized role in an inflammatory reaction following ischemia. It is a fundamental rheological mechanism that may be associated with ischemic injury and reflow injury and it has not been elucidated. To explore the accumulation of granulocytes during myocardial ischemia we studied the accumulation of 111Inlabeled autologous granulocytes in acutely ischemic myocardium during 3 h of flow reduction with and without a subsequent period of reflow in open-chest dogs. Granulocytes accumulated in the ischemic endocardium of all animals and, for the majority of dogs, also in the epicardium. Accumulation in the endocardium was enhanced by reperfusion. The entrapped leukocytes may have an influence on the increase in resistance, since regional accumulation of leukocytes in the endocardium inversely correlated with ischemic blood flow during 3 h of ischemia. The tissue water content measured from the wet and dry weights of biopsies showed a significant positive correlation with the number of entrapped granulocytes. These results suggest that collateral flow is an important mechanism of leukocyte arrival early in ischemic myocardium and that reperfusion enhances granulocyte accumulation.
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Butler, Karyn L., Alice H. Huang, and Judith K. Gwathmey. "AT1-receptor blockade enhances ischemic preconditioning in hypertrophied rat myocardium." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 6 (December 1, 1999): H2482—H2487. http://dx.doi.org/10.1152/ajpheart.1999.277.6.h2482.
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The purpose of this study was to determine whether ischemic preconditioning protects contractile function in hypertrophied rat myocardium from ischemia-reperfusion (I/R) injury. Male salt-sensitive rats were fed a high-salt diet for 2 wk to induce myocardial hypertrophy. Nonhypertrophied hearts were obtained from age-matched Sprague-Dawley (SD) rats fed a regular diet. Heart weight-to-body weight ratios were higher in salt-sensitive rats than in SD rats (6.9 ± 0.2 vs. 4.7 ± 0.2 g/kg, P < 0.01). A second group of salt-sensitive and SD rats was administered losartan (10 mg ⋅ kg−1 ⋅ day−1), an AT1-receptor blocker, for 1 wk before the study. Isolated hearts were preconditioned with transient ischemia before global I/R. After I/R, preconditioned hypertrophied hearts exhibited greater recovery of left ventricular developed pressure compared with that of preconditioned normal hearts (73 ± 8 vs. 18 ± 8%, P < 0.01). Left ventricular developed pressure was further enhanced by losartan in both hypertrophied and normal myocardium (99 ± 5 vs. 73 ± 8%, P < 0.05 and 97 ± 15 vs. 18 ± 8%, P < 0.01). Hypertrophied rat myocardium can be protected from I/R-induced contractile dysfunction by ischemic preconditioning. Losartan improves the ischemic tolerance of normal and hypertrophied myocardium.
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Neely, B. H., and G. R. Hageman. "Differential cardiac sympathetic activity during acute myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 5 (May 1, 1990): H1534—H1541. http://dx.doi.org/10.1152/ajpheart.1990.258.5.h1534.
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Efferent sympathetic activities were simultaneously recorded from two thoracic cardiac nerves in 33 chloralose-anesthetized dogs. Efferent innervation patterns were determined by electrical stimulation prior to recording in each animal. One of the nerves selected for recording was shown to innervate the proposed ischemic region, whereas the other nerve was selected because it was shown to innervate nonischemic regions. Left ventricular ischemia was produced by occlusion of a branch of either the left anterior descending (LAD) or left circumflex (LCX) coronary arteries. Heart rate was paced. Cardiac postganglionic sympathetic efferent activities were recorded during a 30-min coronary occlusion in 22 animals. Thirty minutes after LAD occlusion (n = 10), postganglionic sympathetic activity to ischemic myocardium was decreased (84 +/- 5% of control; P less than 0.05) while activity to nonischemic myocardium was unchanged. Thirty minutes after LCX occlusion (n = 12), postganglionic sympathetic activity to ischemic myocardium was also decreased (87 +/- 3% of control; P less than 0.01); however, sympathetic activity to nonischemic myocardium was increased (159 +/- 10% of control; P less than 0.001). Thus, in the anesthetized canine, regional left ventricular ischemia elicits differential sympathetic neural responses that are dependent on the location of the ischemic myocardium as well as the efferent destinations of the nerves. Changes in cardiac postganglionic sympathetic efferent activities are characterized by decreased activity to ischemic regions, with either no change or increased activity to nonischemic regions.
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Pagel, Paul S., Douglas A. Hettrick, Dermot Lowe, John P. Tessmer, and David C. Warltier. "Desflurane and Isoflurane Exert Modest Beneficial Actions on Left Ventricular Diastolic Function during Myocardial Ischemia in Dogs." Anesthesiology 83, no. 5 (November 1, 1995): 1021–35. http://dx.doi.org/10.1097/00000542-199511000-00016.
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Abstract Background Volatile anesthetics exert cardioprotective effects during myocardial ischemia. This investigation examined the regional systolic and diastolic mechanical responses to brief left anterior descending coronary artery (LAD) occlusion in the central ischemic zone and in remote normal myocardium in the conscious state and during desflurane and isoflurane anesthesia.
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Vismont, F. I., S. N. Chepelev, and P. F. Jushkevich. "Peripheral M-choline-reactive systems in the infarct-limited effect implementation of remote ischemic postconditioning during ischemia-reperfusion of myocardium in experiment." Proceedings of the National Academy of Sciences of Belarus, Medical series 16, no. 4 (December 5, 2019): 424–33. http://dx.doi.org/10.29235/1814-6023-2019-16-4-424-433.
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The search for new effective methods to prevent or mitigate ischemic myocardial damage and the mechanisms for their realization is an important task of modern experimental and clinical medicine. The aim of the study was to elucidate the significance of peripheral M-choline-reactive systems in the realization of the cardioprotective effects of remote ischemic postconditioning (RIPostC) during ischemia-reperfusion of myocardium in experiment. The study revealed that RIPostC has an infarct-limiting effect during ischemia-reperfusion of myocardium in young and old rats, but under the conditions of systemic action of atropine (2 mg/kg), the infarct-limiting effect of RIPostC remained only in old rats. It seems that the activity of peripheral M-choline-reactive systems is important in the mechanisms of realization of the cardioprotective effects of RIPost in young, but not in old rats.
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Kim, Young-Hoon, Yang-Sook Chun, Jong-Wan Park, Chan-Hyung Kim, and Myung-Suk Kim. "Involvement of adrenergic pathways in activation of catalase by myocardial ischemia-reperfusion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 5 (May 1, 2002): R1450—R1458. http://dx.doi.org/10.1152/ajpregu.00278.2001.
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In situ rabbit hearts were subjected to 15 min of regional myocardial ischemia, and at various time points of reperfusion, antioxidant enzyme activity and mRNA expression were measured in ischemic and nonischemic myocardium. Catalase activity increased significantly in both ischemic and nonischemic myocardium, peaking at 1 h after reperfusion and then gradually returning to the control level. Northern blot analysis showed enhanced expression of catalase mRNA in both areas. There were no changes in redox status, because glutathione levels were not altered by ischemia-reperfusion (I/R). We also tested whether catalase activation in the heart results from signaling pathways that might influence not only the heart but also other organs. We found that catalase activity in the brain was increased after myocardial I/R and ischemic stress to the intestine was equipotent to myocardial I/R in catalase activation. We next sought to elucidate the possible involvement of the adrenergic system in catalase stimulation induced by ischemic stimuli. After pretreatment with the α-adrenergic receptor antagonist prazosin, I/R failed to increase catalase activity in the heart and brain. Intravenous norepinephrine increased catalase activity in the heart, brain, and liver. This study shows that brief I/R activates a signaling mechanism to induce catalase activation in multiple organs and the α-adrenergic system is involved as an intermediate pathway in this signal transmission.
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Chepelev, S. N., F. I. Vismont, S. V. Goubkin, and L. N. Maslov. "Cardioprotective efficiency of pharmacological postconditioning using lactic acid in ischemia-reperfusion of the myocardium in rats with transitional hypercholesterolemia." Proceedings of the National Academy of Sciences of Belarus, Medical series 18, no. 2 (June 4, 2021): 135–46. http://dx.doi.org/10.29235/1814-6023-2021-18-2-135-146.
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Cardiovascular disease is the leading cause of death all over the world: for no other reason as many people die every year as from the cardiovascular disease. Taking into account the high medical and social significance of the problem of treating patients with coronary heart disease and acute myocardial infarction, the search for new effective methods of preventing or weakening ischemic myocardial damage and revealing the mechanisms of their implementation is an urgent task of modern experimental and clinical medicine. The aim of the study was to experimentally test the cardioprotective efficiency of pharmacological postconditioning with lactic acid in myocardial ischemia-reperfusion in rats with transient hypercholesterolemia.In the course of the study, it was found that remote ischemic postconditioning (RIPostC) during myocardial ischemia-reperfusion leads to an increase in the level of lactate in the blood and has an infarction-limiting effect in rats. It was revealed that lactate, after injection into the bloodstream of animals at a dose of 10 mg/kg 25 minutes after the start of reperfusion, like RIPostC, leads to a decrease in the necrosis area in the left ventricular of the myocardium. Pharmacological postconditioning with lactate is ineffective in the limiting necrosis area in the myocardium of the left ventricle of rats with transient hypercholesterolemia. The presence of such a risk factor for cardiovascular diseases as hypercholesterolemia can serve as a criterion for excluding the use of pharmacological postconditioning with lactate as a way to reduce ischemic and reperfusion damage to the myocardium in patients with acute myocardial infarction.
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Schwemer, Tjark F., Lukas Radziwolek, Navina Deutscher, Nadine Diermann, Susanne Sehner, Stefan Blankenberg, and Felix W. Friedrich. "Effect of Ranolazine on Ischemic Myocardium IN Patients With Acute Cardiac Ischemia (RIMINI-Trial): A Randomized Controlled Pilot Trial." Journal of Cardiovascular Pharmacology and Therapeutics 24, no. 1 (June 24, 2018): 62–69. http://dx.doi.org/10.1177/1074248418784290.
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Background: Coronary artery disease is the most prevalent manifestation among cardiovascular diseases. Despite modern treatment, risk of ischemic complications in patients with acute coronary syndrome (ACS) remains important. The late Na+ current blocker ranolazine has shown to reduce the risk of recurrent ischemia and worsening of angina in patients with non-ST-segment elevation ACS by possibly improving myocardial perfusion, but up to now no trial has addressed whether this enhanced perfusion also leads to a decrease in ischemic myocardium of patients with ACS. We designed a pilot trial (Reduction of Ischemic Myocardium with Ranolazine-Treatment IN patients with acute myocardial Infarction, ClinicalTrials.gov Identifier: NCT01797484) for feasibility and proof of concept that a 6-week ranolazine add-on therapy would reduce the area of ischemic myocardium in patients with ACS. Methods and Results: The trial was designed in a 2-armed, controlled and randomized way. Twenty participants with unstable angina, proof of acute cardiac ischemia, and myocardial dyskinesia by speckle-tracking echocardiography were included. Ten participants received the study drug ranolazine additionally to standard treatment. The control group received standard treatment without additional study medication. Speckle-tracking echocardiography was performed before coronary intervention, before the first dose of ranolazine, and after 6 weeks of ranolazine treatment. Ranolazine was administered safely during acute myocardial infarction. Speckle-tracking echocardiography proved to be suitable for evaluation of myocardial dyskinesia. Patients receiving ranolazine showed a trend to higher normal fraction of the cumulative global strain than patients in the standard treatment group (15% vs 11%). No major complications relating study medication were observed. Conclusion: In conclusion, in this preliminary hypothesis-driven study, 6-week ranolazine therapy was shown to decrease the area of dyskinetic myocardium in patients with ACS by trend. Global strain rate measurement using speckle-tracking echocardiography can be applied measuring those effects and is, compared to other techniques, safe and harmless. Our data provide a sound basis for a follow-up trial.
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Ji, L. L., R. G. Fu, T. G. Waldrop, K. J. Liu, and H. M. Swartz. "Myocardial response to regional ischemia and reperfusion in vivo in rat heart." Canadian Journal of Physiology and Pharmacology 71, no. 10-11 (October 1, 1993): 811–17. http://dx.doi.org/10.1139/y93-121.
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Ischemia–reperfusion-induced myocardial oxidative changes were investigated in open-chest hearts of anesthetized rats. Surgical occlusion of the left anterior descending coronary artery for 30 min followed by 15 min reperfusion resulted in a significant decrease of reduced glutathione, an increase in glutathione disulfide, and an enhanced lipid peroxidation in rapidly frozen left ventricular tissues. Direct electron paramagnetic resonance spectroscopy revealed an increase in free radical concentration in ischemic cardiac tissues reperfused for 45 s, but the increase diminished at 15 min. These alterations were associated with decreased activities of myocardial glutathione peroxidase, glutathione reductase, and catalase. Ischemia resulted in a significant reduction of high-energy phosphate compounds and an accumulation of nucleotide degradation products, particularly adenosine, in the myocardium. Deterioration of cardiovascular function in reperfused animals was also evident. It is concluded that regional ischemia followed by reperfusion in situ can produce biochemical and physiological alterations consistent with free radical injury in rat hearts, and that an increased purine nucleotide degradation and a decreased antioxidant defense may be responsible for the observed changes.Key words: ischemia–reperfusion, myocardium, oxidative damage, glutathione, antioxidant enzyme.
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Naz, Adiba, and Muntasir Billah. "COVID-19 and Coronary Heart Disease." Encyclopedia 1, no. 2 (April 7, 2021): 340–49. http://dx.doi.org/10.3390/encyclopedia1020028.
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Coronary heart disease (CHD) is the leading cause of mortality worldwide. One of the main contributions of mortality and morbidity in CHD patients is acute myocardial infarction (AMI), which is the result of abrupt occlusion of an epicardial coronary artery due to a sudden rupture of atherosclerotic plaque, causing myocardial ischemia. In the initial stage of myocardial ischemia, lack of oxygen and nutrient supply results in biochemical and metabolic changes within the myocardium. Depletion of oxygen switches the aerobic cellular metabolism to anaerobic metabolism and impairs the oxidative phosphorylation pathway eventually leading to cardiomyocyte death. Several studies suggest an interlink between COVID-19 and ischemic heart disease. An increased ACE2 receptor expression in the myocardium may partly contribute to the myocardial injuries that are observed in patients affected by SARS-CoV-2. Furthermore, pre-existing cardiovascular disease, in conjunction with an aggravated inflammatory response which causes an up-regulation in pro-inflammatory cytokines. Moreover, patients with atherosclerosis are observed to be more prone to ischemic attacks when affected by COVID-19, due to hypercoagulation in the blood as well as elevated pro-inflammatory markers.
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Ristic, Andjelka, Milorad Damjanovic, Branislav Baskot, and Radomir Matunovic. "Stunned myocardium." Vojnosanitetski pregled 62, no. 2 (2005): 165–69. http://dx.doi.org/10.2298/vsp0502165r.
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Background. Stunned myocardium is a state of delayed recovery of regional contractility after a transient period of ischemia followed by reperfusion. Case report. A 67-year-old patient was admitted to our hospital with acute anterior myocardial infarction, and treated using percutaneous transluminal coronary angioplasty (PTCA) within acute disease stage. Reversible myocardial dysfunction persisted after ischemia following the return of normal perfusion. Abnormal resting wall motion with augmentation of contractility at low and high doses of dobutamine characterizes the stunned myocardium and reflects the normal blood flow reserve, characteristic for these postischemic, reperfused segments. SPECT (Single Photon Emission Computerized Tomography) with Tc 99 and dipyradamole showed normalization of perfusion defects in the apical region. Theree months after the infarction and PTCA, contractility was almost completely recovered. Conclusion. Stunned myocardium recovery lasted from few weeks to few months. Control ultrasonography as well as SPECT showed normalization of systolic function of the left ventricle in the viable segments registered at previous examinations.
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Parratt, James R., Agnes Vegh, and Julius Gy Papp. "Bradykinin as an endogenous myocardial protective substance with particular reference to ischemic preconditioning–a brief review of the evidence." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 837–42. http://dx.doi.org/10.1139/y95-114.
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The present brief review summarizes the evidence for the possibility that endogenously released bradykinin plays a major role in protecting the heart against the consequences of acute myocardial injury. This evidence includes the facts that kinins are generated under myocardial ischemia; that when they are administered, they are cardioprotective (e.g., antiarrhythmic); that drugs that enhance the release of bradykinin from the ischemic heart reduce the ischemic injury and, conversely, drugs that block bradykinin receptors attenuate the reduction in ischemic injury resulting from the release of, or administration of, bradykinin. The possible mechanism of bradykinin in the cardioprotection afforded by ischemic preconditioning is summarized. Ischemic preconditioning can be defined as the marked reduction in the severity of ischemic changes that result from coronary artery occlusion when that occlusion is preceded by brief periods of myocardial ischemia, either regional or global, induced, for example, by complete or partial coronary artery occlusion or by rapid ventricular pacing. The possible mechanisms of cardioprotection elicited by bradykinin (and ischemic preconditioning) are summarized. The most likely is the generation of cyclic GMP within the ischemic myocardium following bradykinin-stimulated nitric oxide generation and release from endothelial cells.Key words: endogenous myocardial protective substances, bradykinin, ischemic preconditioning, cardiac arrhythmias, myocardial ischemia.
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Ford, D. A., and R. W. Gross. "Activation of myocardial protein kinase C by plasmalogenic diglycerides." American Journal of Physiology-Cell Physiology 258, no. 1 (January 1, 1990): C30—C36. http://dx.doi.org/10.1152/ajpcell.1990.258.1.c30.
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Recently, we have demonstrated that myocardial sarcolemma is predominantly comprised of plasmalogen molecular species and that the plasmalogen metabolite 1-O-alk-1'-enyl-2-acyl-sn-glycerol (AAG) accumulates during myocardial ischemia despite substantial decreases in 1,2-diacyl-sn-glycerol (DAG) content. To elucidate the physiological significance of AAG accumulation during myocardial ischemia, rabbit myocardial protein kinase C was partially purified by DE-52 and high-performance hydroxylapatite chromatographies, and the potency of AAG as an activator of myocardial protein kinase C was assessed. Both AAG and 1-O-alkyl-2-acyl-sn-glycerol are potent activators of myocardial protein kinase C with obligatory requirements for physiological increments in free Ca2+ concentration. In contrast, a substantial amount of myocardial protein kinase C activity elicited by DAG was calcium independent. Concentration dependence of ATP for protein kinase C-mediated phosphorylation was identical utilizing either ether-linked diglycerides or DAG as activators, with maximal phosphorylation manifest at ATP concentrations two orders of magnitude less than those found in ischemic myocardium. Thus accumulation of AAG in ischemic myocardium in conjunction with increases in intracellular free Ca2+ concentration may synergistically activate protein kinase C and therefore modulate phosphorylation of proteins in specific subcellular loci.
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Summerour, S. R., J. L. Emery, B. Fazeli, J. H. Omens, and A. D. McCulloch. "Residual Strain in Ischemic Ventricular Myocardium." Journal of Biomechanical Engineering 120, no. 6 (December 1, 1998): 710–14. http://dx.doi.org/10.1115/1.2834883.
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Structural remodeling during acute myocardial infarction affects ventricular wall stress and strain. To see whether acute myocardial infarction alters residual stress and strain in the left ventricle (LV), we measured opening angles in rat hearts after 30 minutes of left coronary artery occlusion. The mean opening angle in 18 ischemic hearts (51 ± 20 deg) was significantly greater than in five sham-operated controls (29 ± 11 deg, P < 0.05). To determine whether these alterations in residual strain may be associated with strain softening caused by systolic overstretch of the noncontracting ischemic tissue, we also measured opening angles in isolated hearts that had been passively inflated to high LV pressures (120 mmHg). The mean opening angle of the strain-softened hearts was not significantly different from the sham-operated hearts (34 ± 27 deg, P = 0.74). Mean collagen area fractions in the myocardium were not significantly different between ischemic hearts (0.027 ± 0.014) and the nonischemic group (0.022 ± 0.011). Although there were significant differences in opening angles measured with ischemia, they do not appear to be a result of altered extracellular collagen content or softening associated with overstretch. Thus, there is a significant change in residual strain associated with acute ischemia that may be related to changes in collagen fiber structure, myocyte structure, or metabolic state.
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Stănescu, Alexandra, Diana Opincariu, Nora Rat, Mirabela Morariu, Sebastian Condrea, Imre Benedek, and Theodora Benedek. "Hybrid Imaging in the Assessment of Myocardial Ischemia and Viability." Journal of Interdisciplinary Medicine 1, no. 3 (December 1, 2016): 242–46. http://dx.doi.org/10.1515/jim-2016-0071.
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Abstract Myocardial ischemia results from a reduction in blood flow as a consequence of a coronary stenosis, which produces ischemia in the myocardial territories irrigated by the stenotic artery. Myocardial viability is a concept that derived from several studies in which it was observed that, even if revascularization occurred, an irreversible left ventricular contractile dysfunction remained. The terms “stunned” and “hibernating” myocardium have been traditionally associated with the viable myocardium, and many controversies still exist on the most appropriate method to assess the presence and extent of viable myocardium. During the last decades, many efforts have been made to identify the best method to determine the viability of the myocardial tissue. Due to the fact that none of the stand-alone imaging methods provide sufficient data about myocardial viability, new methods for the investigation of myocardial viability became necessary. Thus, the concept of hybrid imaging was developed, consisting in the association of different imaging techniques, finally resulting in a single image that offers all the details provided by the two isolated methods of diagnosis, therefore being more precise in regards to the identification of viable myocardium territory. This review aims to appraise the recent studies related to myocardial viability investigated with hybrid imaging.
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Mitani, A., K. Kinoshita, K. Fukamachi, M. Sakamoto, K. Kurisu, Y. Tsuruhara, F. Fukumura, A. Nakashima, and K. Tokunaga. "Effects of glibenclamide and nicorandil on cardiac function during ischemia and reperfusion in isolated perfused rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 6 (December 1, 1991): H1864—H1871. http://dx.doi.org/10.1152/ajpheart.1991.261.6.h1864.
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We examined influences of a blocker (glibenclamide) and an opener (nicorandil) of the ATP-sensitive potassium (KATP) channel on extracellular K concentration [( K+]e), as well as the myocardial function and metabolites during global ischemia and reperfusion in Langendorff-perfused rat heart preparation. In control hearts, [K+]e began to rise 20 s after the onset of ischemia up to an initial peak (8.3 +/- 0.3 mM) at 2.5 +/- 0.7 min, then fell to 6.0 +/- 0.8 mM after 8.2 +/- 0.7 min, and then rose progressively to 14.6 +/- 0.8 mM at the end of 30 min of ischemia. Glibenclamide (50 microM) reduced the initial peak of [K+]e to 7.2 +/- 0.3 mM (P less than 0.01), and nicorandil (200 microM) increased it to 9.4 +/- 0.6 mM (P less than 0.01). There were no significant differences in [K+]e values among all groups at the end of ischemia. During ischemia, nicorandil decreased the time to mechanical arrest from 1.9 +/- 0.1 min to 1.5 +/- 0.1 min, whereas it was increased by glibenclamide to 2.7 +/- 0.4 min. In control hearts, the time to onset of ischemic contracture was 14.7 +/- 1.8 min. Nicorandil delayed onset of contracture and glibenclamide accelerated it. Thus we have confirmed that some part of the early increase in [K+]e during ischemia is attributable to K+ efflux through the KATP channel in our model, and opening of the KATP channel may contribute to a rapid reduction of the contractility of the ischemic myocardium that subsequently protects the myocardium against further ischemic injury.
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Kakkar, Rakesh, Dallas P. Seitz, Rani Kanthan, Raju VS Rajala, Jasim M. Radhi, Xinto Wang, Mohammed K. Pasha, Rui Wang, and Rajendra K. Sharma. "Calmodulin-dependent cyclic nucleotide phosphodiesterase in an experimental rat model of cardiac ischemiareperfusion." Canadian Journal of Physiology and Pharmacology 80, no. 1 (January 1, 2002): 59–66. http://dx.doi.org/10.1139/y02-001.
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In the present study, we investigated the activity and expression of calmodulin-dependent cyclic nucleotide phosphodiesterase (CaMPDE) and the effects of calpains in rat heart after ischemia and reperfusion. Immunohistochemical studies indicated that CaMPDE in normal heart is localized in myocardial cells. Rat ischemic heart showed a decrease in CaMPDE activity in the presence of Ca2+ and calmodulin; however, in ischemicreperfusion tissue a progressive increase in Ca2+ and calmodulin-independent cyclic nucleotide phosphodiesterase (CaM-independent PDE) activity was observed. Perfusion of hearts with cell-permeable calpain inhibitor suppressed the increase of Ca2+ and CaM-independent PDE activity. Protein expression of CaMPDE was uneffected by hypoxic injury to rat myocardium. The purified heart CaMPDE was proteolyzed by calpains into a 45 kDa immunoreactive fragment in vitro. Based on these results, we propose that hypoxic injury to rat myocardium results in the generation of CaM-independent PDE by calpain mediated proteolysis, allowing the maintenance of cAMP concentrations within the physiological range.Key words: phosphodiesterase, calmodulin, calpains, heart, ischemia, reperfusion.
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Varnavas, Varnavas C., Konstantinos Kontaras, Chryssoula Glava, Christos D. Maniotis, Michael Koutouzis, Giannis G. Baltogiannis, Apostolos Papalois, Theofilos M. Kolettis, and Zenon S. Kyriakides. "Chronic skeletal muscle ischemia preserves coronary flow in the ischemic rat heart." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 4 (October 2011): H1229—H1235. http://dx.doi.org/10.1152/ajpheart.00232.2011.
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Chronic skeletal muscle ischemia confers cytoprotection to the ventricular myocardium during infarction, but the underlying mechanisms remain unclear. Although neovascularization in the left ventricular myocardium has been proposed as a possible mechanism, the functional capacity of such vessels has not been studied. We examined the effects of chronic limb ischemia on infarct size, coronary blood flow, and left ventricular function after ischemia-reperfusion. Hindlimb ischemia was induced in 65 Wistar rats by excision of the left femoral artery, whereas 65 rats were sham operated. After 4 wk, myocardial infarction was generated by permanent coronary artery ligation. Infarct size was measured 24 h postligation. Left ventricular function was evaluated in isolated hearts after ischemia-reperfusion, 4 wk after limb ischemia. Neovascularization was assessed by immunohistochemistry, and coronary flow was measured under maximum vasodilatation at different perfusion pressures before and after coronary ligation. Infarct size was smaller after limb ischemia compared with controls (24.4 ± 8.1% vs. 46.2 ± 9.5% of the ventricle and 47.6 ± 8.7% vs. 80.1 ± 9.3% of the ischemic area, respectively). Indexes of left ventricular function at the end of reperfusion (divided by baseline values) were improved after limb ischemia (developed pressure: 0.68 ± 0.06 vs. 0.59 ± 0.05, P = 0.008; maximum +dP/d t: 0.70 ± 0.08 vs. 0.59 ± 0.04, P = 0.004; and maximum −dP/d t: 0.86 ± 0.14 vs. 0.72 ± 0.10, P = 0.041). Coronary vessel density was markedly higher ( P = 0.00021) in limb ischemic rats. In contrast to controls ( F = 5.65, P = 0.00182), where coronary flow decreased, it remained unchanged ( F = 1.36, P = 0.28) after ligation in limb ischemic rats. In conclusion, chronic hindlimb ischemia decreases infarct size and attenuates left ventricular dysfunction by increasing coronary collateral vessel density and blood flow.
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Xia, Rui, Bo Zhao, Yang Wu, Jia-Bao Hou, Li Zhang, Jin-Jin Xu, and Zhong-Yuan Xia. "Ginsenoside Rb1 Preconditioning Enhances eNOS Expression and Attenuates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats." Journal of Biomedicine and Biotechnology 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/767930.
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Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (P<0.05). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (P<0.05). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.
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Picard, Sandra, Rene Rouet, Frederic Flais, Pierre Ducouret, Gerard Babatasi, Andre Khayat, Jean-Claude Potier, Henri Bricard, and Jean-Louis Gerard. "Proarrhythmic and Antiarrhythmic Effects of Bupivacaine in an In Vitro Model of Myocardial Ischemia and Reperfusion." Anesthesiology 88, no. 5 (May 1, 1998): 1318–29. http://dx.doi.org/10.1097/00000542-199805000-00024.
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Background Bupivacaine may have toxic cardiovascular effects when accidentally administered by intravascular injection. However, its electrophysiologic effects in the presence of myocardial ischemia remain unknown. The authors evaluated the electrophysiologic and anti- and proarrhythmic effects of bupivacaine in an in vitro model of the ischemic and reperfused myocardium. Methods In a double-chamber bath, a guinea pig right ventricular muscle strip was subjected partly to normal conditions and partly to simulated ischemia followed by reperfusion. The electrophysiologic effects of bupivacaine were studied at 1, 5, and 10 microM concentrations. Results Bupivacaine (5 and 10 microM) decreased the maximal upstroke velocity of the action potential (Vmax) in normoxic conditions and further decreased (10 microM) the Vmax decrease induced by ischemic conditions. Bupivacaine reduced the mean occurrence time to the onset of myocardial conduction blocks (9 +/- 3 min; mean +/- SD; P < 0.005 with 5 and 10 microM, compared with 17 +/- 6 min during simulated ischemia with no drug or control), and it increased the number of preparations that became inexcitable to pacing (55% of preparations, with 1 microM and 100% with 5 and 10 microM, compared with 17% for the control group). The incidence of spontaneous arrhythmias was reduced by 5 and 10 microM bupivacaine during ischemia and reperfusion and was enhanced by 1 microM bupivacaine during the ischemic phase. Conclusions In guinea pig myocardium under ischemic conditions, bupivacaine induced a loss of excitability at concentrations of 5 and 10 microM. Proarrhythmic effects observed at 1 microM were considered as lower than the cardiotoxic range in normoxic conditions. The incidence of reperfusion arrhythmias was decreased at all concentrations.
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Martin, Claus, Rainer Schulz, Heiner Post, Petra Gres, and Gerd Heusch. "Effect of NO synthase inhibition on myocardial metabolism during moderate ischemia." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (June 1, 2003): H2320—H2324. http://dx.doi.org/10.1152/ajpheart.01122.2002.
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Nitric oxide (NO) is involved in the control of myocardial metabolism. In normoperfused myocardium, NO synthase inhibition shifts myocardial metabolism from free fatty acid (FFA) toward carbohydrate utilization. Ischemic myocardium is characterized by a similar shift toward preferential carbohydrate utilization, although NO synthesis is increased. The importance of NO for myocardial metabolism during ischemia has not been analyzed in detail. We therefore assessed the influence of NO synthase inhibition with N G-nitro-l-arginine (l-NNA) on myocardial metabolism during moderate ischemia in anesthetized pigs. In control animals, the increase in left ventricular pressure with l-NNA was mimicked by aortic constriction. Before ischemia, l-NNA decreased myocardial FFA consumption (MV˙FFA; P < 0.05), while consumption of carbohydrate and O2 (MV˙o 2) remained constant. ATP equivalents [calculated with the assumption of complete oxidative substrate decomposition (ATPeq)] decreased withl-NNA ( P < 0.05), associated with a decrease of regional myocardial function ( P < 0.05). In contrast, aortic constriction had no effect on MV˙FFA, while MV˙o 2increased ( P < 0.05) and ATPeq and regional myocardial function remained constant. During ischemia, alterations in myocardial metabolism were similar in control and l-NNA-treated animals: MV˙FFAdecreased ( P < 0.05) and net lactate consumption was reversed to net lactate production ( P < 0.05). Regional myocardial function was decreased ( P < 0.05), although more markedly in animals receiving l-NNA ( P < 0.05). We conclude that the efficiency of oxidative metabolism was impaired by l-NNA per se, paralleled by impaired regional myocardial function. During ischemia, l-NNA had no effect on myocardial substrate consumption, indicating that NO synthases were no longer effectively involved in the control of myocardial metabolism.
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Jennings, Robert B., Charles E. Murry, and Keith A. Reimer. "Preconditioning myocardium with ischemia." Cardiovascular Drugs and Therapy 5, no. 5 (October 1991): 933–38. http://dx.doi.org/10.1007/bf00053555.
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Tanhehco, Elaine J., Koji Yasojima, Patrick L. McGeer, Ruth A. Washington, Kenneth S. Kilgore, Jonathon W. Homeister, and Benedict R. Lucchesi. "Preconditioning reduces tissue complement gene expression in the rabbit isolated heart." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 6 (December 1, 1999): H2373—H2380. http://dx.doi.org/10.1152/ajpheart.1999.277.6.h2373.
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Both preconditioning and inhibition of complement activation have been shown to ameliorate myocardial ischemia-reperfusion injury. The recent demonstration that myocardial tissue expresses complement components led us to investigate whether preconditioning affects complement expression in the isolated heart. Hearts from New Zealand White rabbits were exposed to either two rounds of 5 min global ischemia followed by 10 min reperfusion (ischemic preconditioning) or 10 μM of the ATP-dependent K+(KATP) channel opener pinacidil for 30 min (chemical preconditioning) before induction of 30 min global ischemia followed by 60 min of reperfusion. Both ischemic and chemical preconditioning significantly ( P < 0.05) reduced myocardial C1q, C1r, C3, C8, and C9 mRNA levels. Western blot and immunohistochemistry demonstrated a similar reduction in C3 and membrane attack complex protein expression. The KATPchannel blocker glyburide (10 μM) reversed the depression of C1q, C1r, C3, C8, and C9 mRNA expression observed in the pinacidil-treated hearts. The results suggest that reduction of local tissue complement production may be one means by which preconditioning protects the ischemic myocardium.