Relevant bibliographies by topics / Myocardium. Ischemia

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Myocardium. Ischemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Myocardium. Ischemia.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Myocardium. Ischemia"

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Myocardium. Ischemia"

1

Du, Ying. "Ischemic and pharmacological preconditioning of rat myocardium : effects on ischemia-reperfusion injury /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20DU.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Ko, Robert K. M. "Molecular aspects of myocardial ischemia/reperfusion injury and the protective effects of allopurinol." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30699.

Full text
Abstract:
A growing body of evidence has now accumulated supporting the involvement of oxygen-derived free radicals in the development of myocardial ischemia/reperfusion (I/R) injury. We have, therefore, undertaken the present study to examine (1) I/R-related alterations in myocardial antioxidant capacity in pentobarbital anesthetized open-chest rabbits subjected to left circumflex coronary artery ligation followed by reperfusion; (2) the protective effects of pretreatrnent with allopurinol or the 21-aminosteroid U74006F; (3) alternative mechanisms to xanthine oxidase inhibition for allopurinol protection against I/R injury; and (4) the effect of allopurinol treatment on the antioxidant capacity of erythrocytes in pigs used in a heart-lung transplantation study. In the rabbit myocardium, a marked impairment in myocardial antioxidant capacity developed in association with the onset of irreversible injury, as reflected in the enhancement in glutathione (GSH) depletion and formation of thiobarbituric acid-reactive substances (TBARS) following in vitro incubation of tissue homogenate with tert-butylhydroperoxide (TBHP). During the course of post-ischemic reperfusion, the protracted time-course of alterations in antioxidant capacity dissociated them from the early burst of radical formation known to occur at the onset of post-ischemic reperfusion of the myocardium. When the time-dependent changes in functional indices of antioxidant status (TBHP-induced GSH depletion and formation of TBARS) were analysed in relation to activities of antioxidant enzymes, evidence suggestive of functionally relevant impairments in Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and glutathione reductase (GRD) activities was found. These results and our demonstration of significant decreases in the activity of GSH-dependent antioxidant enzymes under acidotic conditions suggest that a transient impairment in the functioning of antioxidant enzymes may be involved in triggering irreversible myocardial I/R injury. Repetitive brief episodes of I/R produced a progressive decrease in myocardial ATP levels, which was not associated with any detectable changes in myocardial antioxidant capacity. Ischemic preconditioning produced by brief episodes of I/R did not affect the severity of subsequently induced I/R injury. These results suggest that brief episodes of myocardial ischemia do not produce oxidative tissue damage and the ischemia-induced depletion in myocardial ATP level is at least partially dissociable from the I/R-related impairment in tissue antioxidant capacity. Isolated Langendorff-perfused rabbit hearts subjected to I/R did not show any changes in antioxidant capacity. However, when intact hearts were subjected to ischemia in vivo and a subsequent reperfusion in vitro, an impairment in myocardial antioxidant capacity became apparent. These results suggest that blood elements, possibly activated neutrophils, may be a crucial factor involved in the development of I/R-induced oxidant injury. Chronic allopurinol pretreatment (1 mg/ml in drinking water or approximately 75 mg/kg/day) for 7 days prior to ischemia provided significant protection against I/R-induced alterations in myocardial antioxidant capacity, but not the decrease in tissue ATP levels. This chronic allopurinol regimen was found to enhance myocardial GRD activity in nonischemic tissue. In addition, both allopurinol and oxypurinol inhibited the transition metal ion-catalysed ascorbate oxidation and lipid peroxidation in vitro, likely as a consequence of their metal chelating properties. Similarly, myoglobin-TBHP-catalysed oxidation of uric acid and lipid peroxidation were also suppressed by allopurinol. All these suggest that allopurinol may favorably alter myocardial antioxidant capacity directly by virtue of its transition metal chelating properties and its antioxidant actions in myoglobin-mediated oxidative processes. The acute administration of 21-aminosteroid U74006F (3 mg/kg, i.v) under conditions comparable to those known to protect against trauma-induced damage in the central nervous system failed to reduce manifestations of oxidative injury in rabbit hearts subjected to ischemia and reperfusion. Although reactive oxy-radicals have been implicated in both types of tissue damage, the observed difference in susceptibility to protection by this steroidal antioxidant suggests that the molecular mechanisms involved are not identical. In the heart-lung transplantation study, erythrocytes from allopurinol-treated pigs (given repeatedly at an oral dose of 50 mg/kg) showed a time/dose-dependent increase in antioxidant capacity as reflected in the decrease in malondialdehyde production following in vitro oxidative challenge. The extent of red cell protection in both donor and recipient animals correlated significantly with the functional viability of the transplanted lung tissue, as assessed by tissue water content. These results suggest that the measurement of erythrocyte antioxidant capacity may provide an useful assessment of generalized alterations in tissue antioxidant status produced by pharmacological interventions.
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
APA, Harvard, Vancouver, ISO, and other styles
3

Löwbeer, Christian. "Cardiac troponin T in clinical and experimental studies /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-426-6/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Bhimji, Shabir. "Myocardial ischemic injury in experimental diabetes." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25562.

Full text
Abstract:
The nature and extent of myocardial ischemic injury (Mil) produced either by coronary artery ligation/reperfusion or by injection of isoproterenol (ISO) was studied in the 10-week alloxan-diabetic rabbit. Prior to the induction of ischemic injury, investigation of the left ventricles of the diabetic rabbit after 10-weeks revealed significant magnesium depletion and inhibition of myofibrillar and sarcoplasmic reticulum ATPase activities. In addition, the activity of the lysosomal enzyme, N-acetyl-β-glucosaminidase was significantly increased in diabetic left ventricular homogenates. Ultrastructural studies revealed significant lipid and glycogen accumulation, dilatation of the sarcoplasmic reticulum and damage to the mitochondria in left ventricles of the diabetic animals. Administration of ISO to both control and diabetic animals resulted in atrial tachycardias and ventricular fibrillation. The severity of the arrhythmias and the overall mortality was the same in both groups of animals. Serum analyses revealed significantly greater increases in blood glucose, free fatty acids, total cholesterol and creatine kinase activity in the ISO-treated diabetic animals relative to ISO-treated controls. ISO treatment of both control and diabetic animals produced similar increases in heart weight, left ventricular weight and myocardial water content. Analyses of various subcellular organelle marker enzyme activities indicated a significantly greater decrease in the K⁺ ,Ca²⁺ -stimulated sarcoplasmic reticulum ATPase of ISO-treated diabetic animal hearts. In addition, significantly greater increases in Ca and hydroxyproline and decreases in the levels of ATP were evident in the ISO-treated diabetic animal hearts. Ultra-structural studies revealed significant damage to the mitochondria in both ISO-treated control and diabetic hearts, the magnitude of the damage being greater in the diabetic animals. Mitochondria from both groups of animals showed swelling and fragmentation, myofibrils appeared as a homogeneous mass and did not show the characteristic Z-lines. Glycogen depletion and lipid accumulation was observed in both groups of animals. In addition, both groups of animals showed amorphous dense bodies in the mitochondria after ISO-treatment. After 40-minutes occlusion of the left circumflex coronary artery followed by 60-minutes of reperfusion, hemodynamic measurements revealed significant decreases in the left ventricular and systemic arterial pressures in the diabetic animals relative to controls. Analyses of subcellular organelle enzymes from the ischemic tissue revealed that sarcolemmal Na⁺ ,K⁺ -ATPase, mitochondrial ATPase and sarcoplasmic reticulum ATPase activities were decreased after coronary occlusion in both control and diabetic animals. However, upon reperfusion, unlike the control, no recovery of the mitochondrial ATPase was observed in the diabetic animals. In addition, a further depression of both the sarcolemmal and sarcoplasmic reticulum ATPase activities were seen in the diabetic animals compared to controls on reperfusion. Ion measurements revealed a significant accumulation of calcium in both control and diabetic animals, the magnitude of the increase being greater in the diabetic animals. Similarly, both tissue ATP levels and the ability of the mitochondria to generate ATP were depressed in the diabetic animals as compared to controls following coronary artery occlusion and reperfusion. Following coronary artery ligation and reperfusion, the diabetic animals showed a significantly higher incidence of ventricular fibrillation and cardiogenic shock as compared to controls. Ultrastructural studies revealed myocardial damage to both control and diabetic hearts following coronary artery ligation and reperfusion. However, the diabetic myocardium showed a higher incidence and frequency of hypercontraction bands, an increase in the amorphous dense bodies and slightly greater damage to the mitochondria. Coronary artery ligation in conscious control, 6 and 12 week-diabetic rats resulted in post-ligation arrhythmias (especially ventricular fibrillation), the incidence of which was much greater in the diabetic animals. The mortality rate of 12-week diabetic rats undergoing coronary ligation was 100% within 1-7 minutes following ligation. No differences in occluded or infarcted zones of the surviving 6-week diabetic and control rats were detected. Analyses of ionic composition revealed a significant magnesium deficiency in the diabetic hearts as compared to controls. These data indicate that the diabetic animals show a greater susceptibility of the myocardium to ischemic injury. Although numerous metabolic and chemical alterations are present in the diabetic myocardium, it is possible that magnesium deficiency may be a factor determining the higher incidence of arrhythmias and ischemic injury in diabetic animals.
Pharmaceutical Sciences, Faculty of
Graduate
APA, Harvard, Vancouver, ISO, and other styles
5

Nagra, Aarondeep Singh. "Investigation into the cardiotoxic effects of β-adrenergic receptor agonists in myocardial ischaemia/reperfusion injury." Thesis, Coventry University, 2016. http://curve.coventry.ac.uk/open/items/5dbd924b-a29f-4281-9f7c-bc14351cc294/1.

Full text
Abstract:
The treatment of asthma still relies on primary therapy with bronchodilators; in particular β adrenergic receptor (bAR) agonists with a diverse range of short acting and long acting βARs available. An increase in the number of cardiovascular events with the use of bronchodilators have recently been reported including hypertrophy, heart failure, myocardial ischaemia and infarction. Several subtypes of βAR receptors exist including the β1 Adrenergic Receptor (β1AR) and β2 Adrenergic Receptor (β2AR), both located in the heart. The effects of selective β2AR agonists were investigated in the Langendorff model of myocardial ischaemia reperfusion injury, isolated perfused rat hearts underwent 35 minutes of ischaemia and 120 minutes of reperfusion. The selective β2AR long acting β agonists Formoterol and Salmeterol had no significant effect on infarct to risk ratio or time taken to depolarisation and hypercontracture in isolated cardiomyocytes. The non-selective β1AR agonist Isoproterenol has been show to induce myocardial ischaemia and infarction in rat hearts previously, here we demonstrated Isoproterenol (0.5μM) significantly decreased time taken to depolarisation and hypercontracture in isolated cardiomyocytes. The short acting β2AR agonist Salbutamol (0.01μ-1μM) significantly increased infarct to risk ratio in the Langendorff in addition to significantly decreasing time to hypercontracture in cardiomyocytes in the oxidative stress model highlighting a potential role of the mitochondrial permeability transition pore (mPTP). Activation of phosphorylated Akt and phosphorylated Erk1/2 via the PI3K/Akt signalling pathway and p44/p42 MAPK pathway were investigated by western blot analysis. Salbutamol significantly elevated expression of p-Akt in rat hearts exposed to reperfusion for 20 and 120 minutes whilst reducing expression of p-Erk. Recorded elevated cleaved caspase 3 expression in Salbutamol treated hearts can be associated as a marker of increased in cardiomyocyte cell death. The β1AR antagonist CGP 20712 was administered in the presence of Salbutamol with minimal reduction in infarct size in rat hearts recorded and no significant change in time taken to hypercontracture in isolated cardiomyocytes suggesting that Salbutamol mediated toxicity is via β2AR activation. Confirmation of this was verified with the β2AR antagonist ICI 118, 551. Significant decrease in infarct size was recorded in addition to a significant increase in time to hypercontracture in the oxidative stress model. Further to this, caspase 3 expression was significantly reduced in addition with p-Akt expression. With a potential role of the mitochondria and the mPTP contributing to Salbutamol induced myocardial injury, the Cyclophilin D inhibitor Cyclosporin A was administered in hearts and cardiomyocytes in the presence of Salbutamol. Infarct size was significantly reduced whilst time taken to hypercontracture significantly increased, suggesting that CsA treatment inhibits Salbutamol mediated injury via Cyclophilin D inhibition of the mPTP. To conclude, our results demonstrated that Salbutamol caused cardiotoxicity at tissue, cellular and protein level in conditions of ischaemia reperfusion injury. Further to this, inhibition of Cyclophilin D by CsA, or the use of the β2AR antagonist ICI 118, 551 inhibits Salbutamol induced toxicity.
APA, Harvard, Vancouver, ISO, and other styles
6

Al-Rajaibi, Hajar M. "The role of caspase inhibitors in protecting the myocardium from ischemia reperfusion injury." Thesis, Coventry University, 2008. http://curve.coventry.ac.uk/open/items/7c1324d7-8e28-3a1c-009c-fc7aa0d874f8/1.

Full text
Abstract:
Rapid restoration of blood flow to ischemic myocardium is essential, however it causes further injury called reperfusion injury. Apoptosis contributes significantly to cardiomyocyte cell death during ischemia reperfusion injury, in which caspase family proteases play an essential role as they are the executioners of apoptosis. Caspase inhibitors showed promising cardioprotective results when administered before ischemia or at the start of reperfusion. However, before applying them in pre clinical studies of myocardial ischemia, several investigations needed to be taken to determine their therapeutic window post reperfusion, their effect on functional recovery of myocardium post ischemia, their mechanism of action. Methods Isolated perfused rat hearts were subjected to 35 min ischemia followed by 2 hr reperfusion where caspase inhibitors [broad spectrum caspase inhibitor (ZVAD, 0.1µM), specific caspase 3 inhibitor (DEVD, 0.07µM)] were added at the start of reperfusion, 15, 30 and 60 min after starting reperfusion at the presence or absence of Wortmannin (WORT, 100nM, PI3-kinase inhibitor). Hearts underwent triphenyl tetrazolium staining for infarct size assessment, or were frozen for Western blot analysis. Freshly isolated adult rat ventricular myocytes were subjected to 6 hr hypoxia followed by either 18 hr, where caspase inhibitors (ZVAD, 25µM and DEVD, 25µM) were added at the start of reoxygenation, 15, 30 and 60 min after starting reoxygenation at the presence or absence of Wortmannin (WORT, 100nM). Cardiomyocytes were analysed for viability, apoptosis, necrosis and intracellular caspase-3 activity using flow cytometry analysis. Isolated adult rat ventricular papillary muscles were subjected to 35 min hypoxia followed by 100 min reperfusion where caspase inhibitors [ZVAD (0.1 µM, 2.5µM) and DEVD (2.5µM)] were added at the start of reperfusion throughout. Power output was measured using work loop technique.
APA, Harvard, Vancouver, ISO, and other styles
7

Siu, Ada Hoi Ling. "Cardioprotective effects of herba cistanche on ischemia/reperfusion injury ex vivo and oxidative injury in vitro /." View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BICH%202008%20SIU.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Whittaker, Ross J. "New roles for alpha B-crystallin in protecting the myocardium from ischemia/reperfusion injury." Diss., [La Jolla] : [San Diego] ; University of California, San Diego ; San Diego State University, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3336476.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Tang, Wai-ho Jack, and 鄧偉豪. "Role of polyol pathway in ischemic and hyperglycemic cardiomyopathy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45197404.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Hasanally, Devin. "Bioactive oxidized phosphatidylcholines cause apoptotic cell death in cardiomyocytes during ischemia reperfusion." Springer-Verlag New York, 2014. http://hdl.handle.net/1993/30363.

Full text
Abstract:
The main treatment for myocardial infarction is early reperfusion of ischemic tissue. Ischemia and reperfusion (IR) produces reactive oxygen species that oxidize membrane phospholipids. The production of oxidized lipids and their role on cell death in cardiac IR injury is unknown. Using in vitro model of IR, our goal was to identify oxidized phosphatidylcholines (OxPC) from cardiomyocytes, to determine their bioactivity on cardiomyocyte viability and mitochondrial permeability, and using an OxPC specific EO6 antibody inhibit OxPC activity on cardiomyocytes. Rat cardiomyocytes were exposed to IR and lipid extracts underwent lipidomic analysis with HPLC-MS/MS to quantitate 82 novel OxPC species. Cell viability and mitochondrial permeability were determined in vehicle control, non-oxidized control PC, and fragmented OxPC molecules. EO6 antibody was applied and cell viability was assessed. Cardiomyocytes under IR demonstrated increased relevant OxPCs particularly fragmented species. OxPC treatment resulted in loss of cardiomyocyte viability, increased mitochondrial permeability when compared to control. EO6 antibody blocked the loss of cardiomyocyte viability. We have shown for the first time that OxPCs are generated cardiomyocytes during IR and they have detrimental effects on cardiomyocyte viability. Additionally the EO6 antibody inhibits the bioactivity of the OxPCs on cardiomyocytes and could be part of a future treatment regimen.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Myocardium. Ischemia"

1

Bachinsky, Victor, Oleh Ya Vanchulyak, Alexander G. Ushenko, Yurii A. Ushenko, Alexander V. Dubolazov, Alexander Bykov, Benjamin Hogan, and Igor Meglinski. Multi-parameter Mueller Matrix Microscopy for the Expert Assessment of Acute Myocardium Ischemia. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1450-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Dhalla, Naranjan S., Ian R. Innes, and Robert E. Beamish, eds. Myocardial Ischemia. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2055-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Cokkinos, Dennis V., Constantinos Pantos, Gerd Heusch, and Heinrich Taegtmeyer, eds. Myocardial Ischemia. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-28658-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Kukreja, Rakesh C., and Michael L. Hess. Heat shock proteins in myocardial protection. Georgetown, Tex., USA: Landes Bioscience, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Silent myocardial ischemia. London: Martin Dunitz, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Morganroth, Joel, and E. Neil Moore, eds. Silent Myocardial Ischemia. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1745-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Silent myocardial ischemia and infarction. 3rd ed. New York: Dekker, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Silent myocardial ischemia and infarction. New York: Dekker, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Silent myocardial ischemia and infarction. 2nd ed. New York: Dekker, 1989.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Dhalla, Naranjan S., Nobuakira Takeda, Manjeet Singh, and Anton Lukas, eds. Myocardial Ischemia and Preconditioning. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0355-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Myocardium. Ischemia"

1

Nayler, W. G., W. J. Sturrock, and S. Panagiotopoulos. "Calcium Antagonism and the Ischemic Myocardium." In Myocardial Ischemia, 285–96. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2055-5_24.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Jennings, Robert B., Charles E. Murry, and Keith A. Reimer. "Preconditioning Myocardium with Ischemia." In Stunning, Hibernation, and Calcium in Myocardial Ischemia and Reperfusion, 154–65. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4613-1517-9_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Murry, Charles E., Robert B. Jennings, and Keith A. Reimer. "Preconditioning with Ischemia: A Means to Delay Cell Death in Ischemic Myocardium." In Myocardial Ischemia, 11–20. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2055-5_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Leor, J., and R. A. Kloner. "The hibernating myocardium." In Myocardial Ischemia: Mechanisms, Reperfusion, Protection, 453–62. Basel: Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-8988-9_27.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Godfraind, T. "Action of Calcium Antagonists on the Contraction of Isolated Human Coronary Arteries and Myocardium." In Myocardial Ischemia, 325–38. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2055-5_27.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Poole-Wilson, P. A., and M. A. Tones. "Inability of Superoxide Dismutase and Catalase to Inhibit Calcium Influx on Reoxygenation of Rabbit Myocardium." In Myocardial Ischemia, 123–31. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2055-5_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Ferrari, Roberto, Federica Ferrari, Massimo Benigno, Patrizia Pepi, and Odoardo Visioli. "Hibernating myocardium: Its pathophysiology and clinical role." In Myocardial Ischemia and Reperfusion, 195–99. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4979-6_23.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Vatner, Dorothy E., and Stephen F. Vatner. "Physiological and biochemical adrenergic regulation of the stunned myocardium." In Myocardial Ischemia and Reperfusion, 131–37. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4979-6_16.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Ausma, J., F. Thoné, G. D. Dispersyn, W. Flameng, J. L. Vanoverschelde, F. C. S. Ramaekers, and M. Borgers. "Dedifferentiated cardiomyocytes from chronic hibernating myocardium are ischemia-tolerant." In Myocardial Ischemia and Reperfusion, 159–68. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4979-6_19.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Schömig, A., G. Richardt, and Th Kurz. "Sympatho-adrenergic activation of the ischemic myocardium and its arrhythmogenic impact." In Myocardial Ischemia and Arrhythmia, 117–43. Heidelberg: Steinkopff, 1994. http://dx.doi.org/10.1007/978-3-642-72505-0_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Myocardium. Ischemia"

1

Monich, Victor A., Olga V. Drugova, Valery F. Lazukin, and Anna B. Bavrina. "Low-power light and isolated rat hearts after ischemia of myocardium." In BiOS, edited by Michael R. Hamblin, Ronald W. Waynant, and Juanita Anders. SPIE, 2010. http://dx.doi.org/10.1117/12.840841.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Falk, E. A. "UNSTABLE ANGINA PECTORIS: PATHOLOGIC ASPECTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643711.

Full text
Abstract:
Unstable angina pectoris represents a common and important manifestation of acute ischemic heart disease encompassing the broad spectrum of clinical syndromes between stable effort angina and acute myocardial infarction. This group of patientsisfar from uniform concerning underlying pathogenetic mechanisms and prognosis, but generally the risk of infarction or deathis increased during the unstable period. Most patients are presenting with new or worsening effort angina or angina at rest,and especially patients with rest anginaassociated with transient ECG changes seem to constitute a high risk subgroup. Transient reductions in coronary blood flow,rather than increases in myocardial oxygen demand, seem to play the major role in rest angina, indicating an underlying 'dynamic' coronary stenosis.Furthermore, unstable angina seems to beagood clinicalmarker for actively progressing coronary-artery disease.Pathologically, a rapidly evolving coronary-artery lesion represented by a disrupted atherosclerotic plaque with variable degree of plaque hemorrhage and luminalthrombosis usually is present in patientscoming to autopsy after a period of rest angina. The thrombus at the rupture site may be mural and limited (just sealing therupture) or occlusive depending on the degree of preexisting atherosclerotic stenosis. An occlusive thrombus is seldom seen over ruptured plaques causing less tha15% stenosis (histologic area stenosis), but is found with increasing frequency when stenosis severety increases beyond 15%.Most occlusive thrombi have a layered structure with thrombus material of differing age indicating an episodic growth by repeated mural deposits. Aggregated platelets usually can be identified in the mostrecent part of the thrombus, while older parts are more homogeneous due to fibrin infiltration/stabilization. Additionally,microemboli and microinfarcts are frequently found in the myocardium downstream tocoronary thrombi. So, the period of unstable angina preceding a fatal heart attackseems to be characterized by an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation alternates with intermittent thrombus fragmentation and peripheral embolization. Such a dynamic thrombosis (with or without a concomitant focal vasospastic phenomenon) at the site of an unstable (ruptured) atherosclerotic lesion obviously may lead to the other clearly thrombus-related acute ischemic events: myocardial infarction or sudden death.Clinical studies using coronary angiography and coronary angioscopy during the acute phase of unstable angina have revealed a high frequency of ulcerated (unstable) atherothrombotic lesion in arteries responsible for the acute ischemia. Furthermore, episodic platelet activation (usually associated with chest pain) has recently been demonstrated in patients with unstable angina.The mechanism underlying pain/ischemia(predominantly spasm?) and the rapid plaque progression (plaque hemorr.hage/luminal thrombosis?) during unstable angina maydiffer. Accordingly, therapy directed against a possible spasm (nitrates, calcium antagonists) usually relieves pain effectively without having any documented effect on infarction/survival, while antithr-ombotic therapy (aspirin, heparin) clearlyimproves the prognosis without apparent antianginal effect. Therefore, with the objective not only of relieving pain but also of improving the prognosis, more attention should be paid to the potentially fatal thrombotic process that apparently isgoing on in a major coronary artery of many patients with unstable angina.
APA, Harvard, Vancouver, ISO, and other styles
3

Апарцин, Константин, and Konstantin Apartsin. "The results of fundamental and translational research carried out In the Department of Biomedical Research and Technology of the SBRAS INC in 2012-2016." In Topical issues of translational medicine: a collection of articles dedicated to the 5th anniversary of the day The creation of a department for biomedical research and technology of the Irkutsk Scientific Center Siberian Branch of RAS. Москва: INFRA-M Academic Publishing LLC., 2017. http://dx.doi.org/10.12737/conferencearticle_58be81eca22ad.

Full text
Abstract:
The results of basic and translational research of the Department of Biomedical Research and Technology of Irkutsk Scientific Center of the Siberian Branch of the Russian Academy of Sciences in 2012–2016 The paper presents the results of interdisciplinary research carried out in 2012–2016. The review includes the study of molecular mechanisms of pathogenesis of reparative regeneration, experimental substantiation of methods of diagnosis and prognosis of systemic disturbances of regeneration process, carrying out clinical trials of medicinal products and the formation of observational studies in the field of personalized medicine, the preparation of practical recommendations on the testing of previously developed surgical methods of prevention or correction of postoperative recovery disorders. New data are obtained on the role of the MAP-kinase cascade in the process of regeneration of muscle tissue. It has been established, that with a significant increase of VEGF concentration at the site of the repair of ischemic myocardium, progenitor cells with the CD34+CD45+ phenotype appear, which opens up prospects for the development of biotechnology to restore the damaged myocardium with its own pool of progenitor cells. The new data on the role of growth factors in the post-infarction remodeling are found. It has been revealed, that in local increase of selenium concentration low intensity of mineralization of forming callus in the area of the damage is observed and the formation of bone regeneration slows down. Prospects for the use of nanocomposites of elemental selenium for modulation of reparative response are marked. The dynamics of the level of free circulating mitochondrial DNA (mtDNA) of blood in the early stages of experimental dyslipidemia has been studied. Atherogenic blood factors do not have a significant effect on the release of the mtDNA from dyslipidemia target cells. On the model of acute small-focal myocardial ischemia, we revealed the increase in the mtDNA levels. Prospects of broadcast of diagnostic mtDNA monitoring technology in myocardial ischemia have been marked. The mtDNA monitoring was first tested as a molecular risk pattern in acute coronary syndrome. In survived patients, the concentration of freely circulating mtDNA in blood plasma was 164 times lower. The probability of death of the patient with a high level of mtDNA (over 4000 copies/mL) was 50 % (logit analysis). Methodological level of translational research in the ISC SB RAS has increased due to effective participation in international multi-center clinical trials of drugs, mainly direct anticoagulants: fondaparinux, edoksabana, betriksabana. “Feedback broadcast” of the results of clinical trials of p38-kinase inhibitor, was carried out in the process of changing the model (initially – neuropathic pain) for coronary atherosclerosis. Technologies of pharmacogenetic testing and personalized treatment of diseases in the employees of the Irkutsk Scientific Center were applied. Step T2. Previously developed at the Irkutsk State Medical University and the Irkutsk Scientific Center of Surgery and Traumatologies approaches to surgical prevention and medicinal correction of postoperative hyposplenism were translated into practical health care. Thus, these results obtained in different areas of translational medicine will determine scientific topics of the department in future research cycle.
APA, Harvard, Vancouver, ISO, and other styles
4

Drugova, Olga V., Olesya Zhitnikova, Victor A. Monich, and Irina V. Mukhina. "Phototherapeutic effect of low-power red light on processes of lipid peroxidation in myocardium tissues of rats after ischemia." In EOS/SPIE European Biomedical Optics Week, edited by Tiina I. Karu and Rachel Lubart. SPIE, 2000. http://dx.doi.org/10.1117/12.405910.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Xia, Cao, Ma Kewei, Han Bing, Yu Xiaofeng, Qu Shaochun, Sui Dayuan, Pei Jin, and Gu Xinquan. "Protective effects of ischemic preconditioning on myocardial ischemia reperfusion injury." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027906.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Vasilchenko, S. Yu, A. A. Stratonnikov, A. I. Volkova, V. B. Loschenov, E. A. Sheptak, and S. S. Kharnas. "Investigation of myocardial photodynamic revascularization method on ischemic rat myocardium model." In SPIE Proceedings, edited by Valery V. Tuchin. SPIE, 2006. http://dx.doi.org/10.1117/12.697420.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Discher, Dennis, and Adam Engler. "Mesenchymal Stem Cell Injection After Myocardial Infarction Improves Myocardial Compliance." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176754.

Full text
Abstract:
Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSC) into the acutely ischemic myocardium. Two weeks post-infarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were two-fold stiffer than myocardium from non-infarcted animals but softer than myocardium from vehicle-treated infarcted animals. After eight weeks, the following variables were evaluated: MSC engraftment and left ventricular geometry by histologic methods; cardiac function with a pressure-volume conductance catheter; myocardial fibrosis by Masson trichrome staining; vascularity by immunohistochemistry; and apoptosis by TUNEL assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated post-infarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.
APA, Harvard, Vancouver, ISO, and other styles
8

Zhang, Pei, Tieluo Li, Katrina Williams, Shuyin Li, Xufeng Wei, Hosung Son, Pablo Sanchez, Bartley P. Griffith, and Zhongjun J. Wu. "Analysis of Infarct Size on Myocardial Infarction Remodeling." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53117.

Full text
Abstract:
In the United States, over one million patients sustain left ventricular (LV) injury after myocardial infarction (MI). LV remodeling is an adaptive process of hypertrophy that includes infarct expansion, reduced contractility and LV dilation. Progressive enlargement of non-ischemic, hypocontractile myocardium in the adjacent zone (AZ) following the transmural MI has been identified clinically, which contributes to the development post-MI cardiomyopathy in patients. Till now, how the early regional biomechanical and cellular changes, particularly in the AZ, relate to LV remodeling process remains incompletely understood. This study aims to investigate the temporal and/or spatial variations of strain/stress and myocyte size in an ovine model with various MI sizes.
APA, Harvard, Vancouver, ISO, and other styles
9

Moulton, Bart, and Gopal Allada. "Myocardial Ischemia From Tumor Emboli (TE)." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3838.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Киреева, Виктория, Viktoriya Kireeva, Ю. Усольцев, Yu Usolcev, Ж. Капустенская, Zh Kapustenskaya, Е. Кожевникова, et al. "Intermediate results 2016 of a search study of translational diagnostic methods Mitochondrial dysfunction in patients with chronic myocardial ischemia and/or head Brain." In Topical issues of translational medicine: a collection of articles dedicated to the 5th anniversary of the day The creation of a department for biomedical research and technology of the Irkutsk Scientific Center Siberian Branch of RAS. Москва: INFRA-M Academic Publishing LLC., 2017. http://dx.doi.org/10.12737/conferencearticle_58be81ec94893.

Full text
Abstract:
Purpose of the study. To rate prognostic properties of changes in mitochondrial DNA concentration in the blood plasma of patients with chronic cerebral ischemia and ischemic heart disease in relation to the disease and the effectiveness of the therapy. Materials and methods. The study involved patients suffering from coronary heart disease (CHD) and chronic cerebral ischemia (CCI) with stable and unstable atherosclerotic plaques, who have signed informed consent to the data processing within the framework of scientific research. The patients were admitted to the hospital for examination and treatment of CHD and CCI in Cardiology and Neurology Unit of the Hospital of ISC SB RAS. The subjects underwent laboratory and instrumental examination and analysis of the level of free circulating serum mitochondrial DNA by real-time PCR (copies/ml). The examination results considered as satisfactory were compared with the mtDNA levels before and after the treatment. Results. The average value of the mtDNA levels before and after the treatment in patients of neurological and cardiological profile were significantly different: 1 093 686 copies/ml vs 418 046 copies/ml, respectively (p = 0.02). Unlike women, men mtDNA levels statistically significantly (p = 0.03) decreased after the treatment. We revealed statistically significant differences in mtDNA level indicators before and after the treatment, depending on the definition of the series (p = 0.0010) for rank test Kruskal – Wallis test. The results of the proposed research will help to identify prognostic factors of destabilization of cell damage and plaques in endothelial dysfunction, atherosclerosis and its complications, to conduct clinical test of the method for predicting and diagnostics of cellular damage in chronic ischemia on a background of atherosclerosis.
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Myocardium. Ischemia"

1

Zheng, Jinghui. Quercetin for Myocardial Ischemia/Reperfusion Injury: A Preclinical Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0162.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Lu, Liying, Xiaocong Ma, Jinghui Zheng, Lijuan Li, Wenna Yang, Yixuan Kong, and Jie Wang. Quercetin for Myocardial Ischemia Reperfusion Injury: A Protocol for Systematic Review and Meta Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0067.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

QIN, Xiaoyu, Chunai WANG, Jie ZHANG, Shuwei WANG, and Weiqi ZHANG. Effectiveness and safety of electroacupuncture for myocardial protection in cardiopulmonary bypass patients with myocardial ischemia-reperfusion injury：a protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0045.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Pirich, Christian. Long-term survival of patients with ischemic cardiomyopathy and diabetes as compared to those without diabetes undergoing myocardial viability assessment with 18FDG-PET. Science Repository OÜ, February 2019. http://dx.doi.org/10.31487/j.jicoa.2019.01.001.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Schwieger, Alexandra, Kaelee Shrewsbury, and Paul Shaver. Dexmedetomidine vs Fentanyl in Attenuating the Sympathetic Surge During Endotracheal Intubation: A Scoping Review. University of Tennessee Health Science Center, July 2021. http://dx.doi.org/10.21007/con.dnp.2021.0007.

Full text
Abstract:
Purpose/Background Direct laryngoscopy and endotracheal intubation after induction of anesthesia can cause a reflex sympathetic surge of catecholamines caused by airway stimulation. This may cause hypertension, tachycardia, and arrhythmias. This reflex can be detrimental in patients with poor cardiac reserve and can be poorly tolerated and lead to adverse events such as myocardial ischemia. Fentanyl, a potent opioid, with a rapid onset and short duration of action is given during induction to block the sympathetic response. With a rise in the opioid crisis and finding ways to change the practice in medicine to use less opioids, dexmedetomidine, an alpha 2 adrenergic agonist, can decrease the release of norepinephrine, has analgesic properties, and can lower the heart rate. Methods In this scoping review, studies published between 2009 and 2021 that compared fentanyl and dexmedetomidine during general anesthesia induction and endotracheal intubation of surgical patients over the age of 18 were included. Full text, peer-reviewed studies in English were included with no limit on country of study. The outcomes included post-operative reviews of decrease in pain medication usage and hemodynamic stability. Studies that were included focused on hemodynamic variables such as systolic blood pressure, diastolic blood pressure, mean arterial pressure, heart rate, and use of opioids post-surgery. Result Of 2,114 results from our search, 10 articles were selected based on multiple eligibility criteria of age greater than 18, patients undergoing endotracheal intubation after induction of general anesthesia, and required either a dose of dexmedetomidine or fentanyl to be given prior to intubation. Dexmedetomidine was shown to effectively attenuate the sympathetic surge during intubation over fentanyl. Dexmedetomidine showed a greater reduction in heart rate, systolic blood pressure, diastolic blood pressure, mean arterial pressure than fentanyl, causing better hemodynamic stability in patients undergoing elective surgery.Implications for Nursing Practice Findings during this scoping review indicate that dexmedetomidine is a safe and effective alternative to fentanyl during induction of general anesthesia and endotracheal intubation in attenuating the hemodynamic response. It is also a safe choice for opioid-free anesthesia.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Myocardium. Ischemia' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography