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Journal articles on the topic 'Cardiac hypoxia reoxygenation'

Author: Grafiati

Published: 10 March 2023

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1

Zarndt, Rachel, Sarah Piloto, Frank L. Powell, Gabriel G. Haddad, Rolf Bodmer, and Karen Ocorr. "Cardiac responses to hypoxia and reoxygenation in Drosophila." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 11 (2015): R1347—R1357. http://dx.doi.org/10.1152/ajpregu.00164.2015.

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An adequate supply of oxygen is important for the survival of all tissues, but it is especially critical for tissues with high-energy demands, such as the heart. Insufficient tissue oxygenation occurs under a variety of conditions, including high altitude, embryonic and fetal development, inflammation, and thrombotic diseases, often affecting multiple organ systems. Responses and adaptations of the heart to hypoxia are of particular relevance in human cardiovascular and pulmonary diseases, in which the effects of hypoxic exposure can range in severity from transient to long-lasting. This study

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Kehrer, J. P., Y. Park, and H. Sies. "Energy dependence of enzyme release from hypoxic isolated perfused rat heart tissue." Journal of Applied Physiology 65, no. 4 (1988): 1855–60. http://dx.doi.org/10.1152/jappl.1988.65.4.1855.

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There is a sudden release of intracellular constituents upon reoxygenation of isolated perfused hypoxic heart tissue (O2 paradox) or on perfusion with calcium-free medium after a period of hypoxia. Rat hearts were perfused by the method of Langendorff (Pfluegers Arch. 61: 291-332, 1895) with Krebs-Henseleit medium containing 10 mM glucose. Hearts were equilibrated for 30 min, followed by 90 min of hypoxia or 60 min of hypoxia and 30 min of reoxygenation. The massive enzyme release observed upon reoxygenation after 60 min of hypoxia was prevented by infusing 0.5 or 5 mM cyanide 5 min before reo

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Kapelko, Valery I., Vladimir L. Lakomkin, Alexander A. Abramov, et al. "Protective Effects of Dinitrosyl Iron Complexes under Oxidative Stress in the Heart." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/9456163.

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Background. Nitric oxide can successfully compete with oxygen for sites of electron-transport chain in conditions of myocardial hypoxia. These features may prevent excessive oxidative stress occurring in cardiomyocytes during sudden hypoxia-reoxygenation.Aim. To study the action of the potent stable NO donor dinitrosyl iron complex with glutathione (Oxacom®) on the recovery of myocardial contractile function and Ca2+transients in cardiomyocytes during hypoxia-reoxygenation.Results. The isolated rat hearts were subjected to 30 min hypoxia followed by 30 min reoxygenation. The presence of 30 nM

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Şimşek, Gül, and Hilmi Burak Kandilci. "Hypoxia-Reoxygenation Induced Cardiac Mitochondrial Dysfunction." Journal of Ankara University Faculty of Medicine 71, no. 3 (2018): 139–44. http://dx.doi.org/10.4274/atfm.29863.

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Boslett, James, Craig Hemann, Fedias L. Christofi, and Jay L. Zweier. "Characterization of CD38 in the major cell types of the heart: endothelial cells highly express CD38 with activation by hypoxia-reoxygenation triggering NAD(P)H depletion." American Journal of Physiology-Cell Physiology 314, no. 3 (2018): C297—C309. http://dx.doi.org/10.1152/ajpcell.00139.2017.

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The NAD(P)+-hydrolyzing enzyme CD38 is activated in the heart during the process of ischemia and reperfusion, triggering NAD(P)(H) depletion. However, the presence and role of CD38 in the major cell types of the heart are unknown. Therefore, we characterize the presence and function of CD38 in cardiac myocytes, endothelial cells, and fibroblasts. To comprehensively evaluate CD38 in these cells, we measured gene transcription via mRNA, as well as protein expression and enzymatic activity. Endothelial cells strongly expressed CD38, while only low expression was present in cardiac myocytes with i

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Ning, Xue-Han, Shi-Han Chen, Cheng-Su Xu, et al. "Hypothermia preserves myocardial function and mitochondrial protein gene expression during hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 1 (2003): H212—H219. http://dx.doi.org/10.1152/ajpheart.01149.2002.

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Hypothermia before and/or during no-flow ischemia promotes cardiac functional recovery and maintains mRNA expression for stress proteins and mitochondrial membrane proteins (MMP) during reperfusion. Adaptation and protection may occur through cold-induced change in anaerobic metabolism. Accordingly, the principal objective of this study was to test the hypothesis that hypothermia preserves myocardial function during hypoxia and reoxygenation. Hypoxic conditions in these experiments were created by reducing O2 concentration in perfusate, thereby maintaining or elevating coronary flow (CF). Isol

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Wagner, Kay-Dietrich, Vanja Essmann, Karsten Mydlak, et al. "Decreased susceptibility of cardiac function to hypoxia-reoxygenation in renin-angiotensinogen transgenic rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 1 (2002): R153—R160. http://dx.doi.org/10.1152/ajpregu.00491.2001.

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We tested the hypothesis that the renin-angiotensin system (RAS) protects the contractile function of the myocardium against the damaging effect of hypoxia-reoxygenation. For this purpose, the contractility of isolated papillary muscles from wild-type (WT) rats and from rats expressing human renin and angiotensinogen as transgenes (TGR) was compared. After 15 min of hypoxia, peak force (PF) was decreased to 24 ± 5% of the normoxic values in TGR ( n = 10) and to 18 ± 1% in WT rats ( n = 12). PF and relaxation rates recovered completely in TGR but not in WT rats during 45 min of reoxygenation. I

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Ilyas, Ermita I. Ibrahim, Busjra M. Nur, Sonny P. Laksono, et al. "Effects of Curcumin on Parameters of Myocardial Oxidative Stress and of Mitochondrial Glutathione Turnover in Reoxygenation after 60 Minutes of Hypoxia in Isolated Perfused Working Guinea Pig Hearts." Advances in Pharmacological Sciences 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/6173648.

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In cardiovascular surgery ischemia-reperfusion injury is a challenging problem, which needs medical intervention. We investigated the effects of curcumin on cardiac, myocardial, and mitochondrial parameters in perfused isolated working Guinea pig hearts. After preliminary experiments to establish the model, normoxia was set at 30 minutes, hypoxia was set at 60, and subsequent reoxygenation was set at 30 minutes. Curcumin was applied in the perfusion buffer at 0.25 and 0.5 μM concentrations. Cardiac parameters measured were afterload, coronary and aortic flows, and systolic and diastolic pressu

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Battiprolu, Pavan K., and Kenneth J. Rodnick. "Dichloroacetate selectively improves cardiac function and metabolism in female and male rainbow trout." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 10 (2014): H1401—H1411. http://dx.doi.org/10.1152/ajpheart.00755.2013.

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Cardiac tissue from female rainbow trout demonstrates a sex-specific preference for exogenous glucose and glycolysis, impaired Ca2+ handling, and a greater tolerance for hypoxia and reoxygenation than cardiac tissue from male rainbow trout. We tested the hypothesis that dichloroacetate (DCA), an activator of pyruvate dehydrogenase, enhances cardiac energy metabolism and Ca2+ handling in female preparations and provide cardioprotection for hypoxic male tissue. Ventricle strips from sexually immature fish with very low (male) and nondetectable (female) plasma sex steroids were electrically paced

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Endoh, Hiroshi, Takaho Kaneko, Hiro Nakamura, Katsuhiko Doi, and Eiji Takahashi. "Improved cardiac contractile functions in hypoxia-reoxygenation in rats treated with low concentration Co2+." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 6 (2000): H2713—H2719. http://dx.doi.org/10.1152/ajpheart.2000.279.6.h2713.

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An intracellular mechanism that senses decreases in tissue oxygen level and stimulates hypoxia-related gene expression has been reported in various cell types including the cardiac cell. The mechanism can also be activated by Co2+ in normoxia. Thus we investigated the effects of prior chronic oral CoCl2 on mechanical functions of isolated, perfused rat hearts in hypoxia-reoxygenation. In normoxic rats, 43 days of Co2+ administration increased hematocrit from 45 ± 0.3% (control, n = 18) to 51 ± 0.6% ( n = 19). In hypoxia and reoxygenation, Co2+-pretreated hearts exhibited a significantly higher

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Sharikabad, Mohammad Nouri, Jan Magnus Aronsen, Espen Haugen, et al. "Cardiomyocytes from postinfarction failing rat hearts have improved ischemia tolerance." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 3 (2009): H787—H795. http://dx.doi.org/10.1152/ajpheart.00796.2008.

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Altered myocardial Ca2+ and Na+ handling in congestive heart failure (CHF) may be expected to decrease the tolerance to ischemia by augmenting reperfusion Ca2+ overload. The aim of the present study was to investigate tolerance to hypoxia-reoxygenation by measuring enzyme release, cell death, ATP level, and cell Ca2+ and Na+ in cardiomyocytes from failing rat hearts. CHF was induced in Wistar rats by ligation of the left coronary artery during isoflurane anesthesia, after which cardiac failure developed within 6 wk. Isolated cardiomyocytes were cultured for 24 h and subsequently exposed to 4 h

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Buerke, M., A. S. Weyrich, and A. M. Lefer. "Isolated cardiac myocytes are sensitized by hypoxia-reoxygenation to neutrophil-released mediators." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 1 (1994): H128—H136. http://dx.doi.org/10.1152/ajpheart.1994.266.1.h128.

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We exposed isolated rat cardiac myocytes to 20 min of hypoxia followed by 20 min of reoxygenation and observed the effect of supernatants of stimulated neutrophils [polymorphonuclear leukocytes (PMNs)] given at the beginning of reoxygenation. PMN supernatants induced cardiac myocyte injury, which was characterized by a significant (P < 0.01) reduction in cell viability to 53 +/- 3%, vs. 84 +/- 3% in rat myocytes subjected to hypoxia-reoxygenation (H/R) alone. The PMN supernatants also resulted in elevated creatine kinase (CK) activities in the myocyte medium. To examine specific PMN-release

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Eigel, B. N., H. Gursahani, and R. W. Hadley. "ROS are required for rapid reactivation of Na+/Ca2+ exchanger in hypoxic reoxygenated guinea pig ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 3 (2004): H955—H963. http://dx.doi.org/10.1152/ajpheart.00721.2003.

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The cardiac Na+/Ca2+ exchanger (NCX) contributes to cellular injury during hypoxia, as its altered function is largely responsible for a rise in cytosolic Ca2+ concentration ([Ca2+]i). In addition, the NCX in guinea pig ventricular myocytes undergoes profound inhibition during hypoxia and rapid reactivation during reoxygenation. The mechanisms underlying these changes in NCX activity are likely complex due to the participation of multiple inhibitory factors including altered cytosolic Na+ concentration, pH, and ATP. Our main hypothesis is that oxidative stress is an essential trigger for rapid

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Eigel, B. N., H. Gursahani, and R. W. Hadley. "Na+/Ca2+ exchanger plays a key role in inducing apoptosis after hypoxia in cultured guinea pig ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 4 (2004): H1466—H1475. http://dx.doi.org/10.1152/ajpheart.00874.2003.

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Altered Na+/Ca2+ exchanger (NCX) protein expression or activity is thought to contribute to various aspects of cardiac pathology. In guinea pig ventricular myocytes, NCX-mediated Ca2+ entry is almost entirely responsible for Ca2+ overload during hypoxia-reoxygenation. Because Ca2+ overload is a common initiator of apoptosis, the purpose of this study was to test the hypotheses that NCX activity is critically involved in initiating apoptosis after hypoxia-reoxygenation and that hypoxia-reoxygenation-induced apoptosis can be modulated by changes in NCX protein expression or activity. An NCX anti

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Ruhr, Ilan M., Heather McCourty, Afaf Bajjig, Dane A. Crossley, Holly A. Shiels, and Gina L. J. Galli. "Developmental plasticity of cardiac anoxia-tolerance in juvenile common snapping turtles ( Chelydra serpentina )." Proceedings of the Royal Society B: Biological Sciences 286, no. 1905 (2019): 20191072. http://dx.doi.org/10.1098/rspb.2019.1072.

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For some species of ectothermic vertebrates, early exposure to hypoxia during embryonic development improves hypoxia-tolerance later in life. However, the cellular mechanisms underlying this phenomenon are largely unknown. Given that hypoxic survival is critically dependent on the maintenance of cardiac function, we tested the hypothesis that developmental hypoxia alters cardiomyocyte physiology in a manner that protects the heart from hypoxic stress. To test this hypothesis, we studied the common snapping turtle, which routinely experiences chronic developmental hypoxia and exploits hypoxic e

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Seki, S., and K. T. MacLeod. "Effects of anoxia on intracellular Ca2+ and contraction in isolated guinea pig cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 3 (1995): H1045—H1052. http://dx.doi.org/10.1152/ajpheart.1995.268.3.h1045.

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Single, enzymatically isolated guinea pig ventricular myocytes were exposed to 3-min periods of anoxia with glucose-free Tyrode solution containing 1 mM sodium dithionite (Na2S2O4) and were then reoxygenated for 10 min. The myocytes were exposed to rapid applications of 10 mM caffeine during the control, anoxic, and reoxygenation periods. Intracellular Ca2+ concentration ([Ca2+]i) was measured ratiometrically using indo 1 with simultaneous measurements of cell length. The effects of anoxia on Ca2+ were compared with those of hypoxia and metabolic inhibition. The amplitude of the electrically s

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Marsh, J. D., and K. A. Sweeney. "Beta-adrenergic receptor regulation during hypoxia in intact cultured heart cells." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 1 (1989): H275—H281. http://dx.doi.org/10.1152/ajpheart.1989.256.1.h275.

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Regulation of cardiac beta-adrenergic receptors during hypoxia and ischemia is an area of active investigation, with some investigators reporting an increase in sarcolemmal beta-receptor number after ischemia. Previous studies have been limited by the necessity of examining beta-adrenergic receptor properties in membrane preparations from hypoxic or ischemic cardiac tissue and drawing conclusions about receptor localization in intact tissue from the behavior of a fraction of total receptors in membrane populations. As an approach to examining beta-receptor properties under well-defined pathoph

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Fantini, Elisabeth, Pierre Athias, Martine Courtois, Shorheh Khatami, Alain Grynberg, and Annick Chevalier. "Oxygen and substrate deprivation on isolated rat cardiac myocytes: temporal relationship between electromechanical and biochemical consequences." Canadian Journal of Physiology and Pharmacology 68, no. 8 (1990): 1148–56. http://dx.doi.org/10.1139/y90-172.

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The effects of hypoxia and reoxygenation on action potentials (AP), contractions, and certain biochemical parameters were studied in isolated rat ventricular myocytes in monolayer culture in the presence and absence of glucose. Substrate deprivation alone had no influence on the basal properties. In the presence of glucose, a 4-h hypoxic treatment caused only a moderate decrease in AP amplitude and rate. In substrate-free conditions, hypoxia induced a gradual decline in plateau potential level and in AP duration and rate, followed by rhythm abnormalities and a failure of the electromechanical

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Häkli, Martta, Joose Kreutzer, Antti-Juhana Mäki, et al. "Electrophysiological Changes of Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes during Acute Hypoxia and Reoxygenation." Stem Cells International 2022 (December 19, 2022): 1–15. http://dx.doi.org/10.1155/2022/9438281.

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Ischemic heart disease is the most common cardiovascular disease and a major burden for healthcare worldwide. However, its pathophysiology is still not fully understood, and human-based models for disease mechanisms and treatments are needed. Here, we used human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) to model acute ischemia-reperfusion in our novel cell culture assembly. The assembly enables exchange of oxygen partial pressure for the cells within minutes, mimicking acute ischemic event. In this study, hypoxia was induced using 0% O2 gas for three hours and reoxygenat

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Yang, Zhao-Kang, Nick J. Draper, and Ajay M. Shah. "Ca2+-independent inhibition of myocardial contraction by coronary effluent of hypoxic rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 2 (1999): H623—H632. http://dx.doi.org/10.1152/ajpheart.1999.276.2.h623.

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Endothelial cells release agents that influence cardiac contraction. We recently reported that cultured hypoxic endothelial cells release an unidentified factor(s) that inhibits myocardial contraction. In this study, we investigated the effects of coronary effluent of isolated hypoxic rat hearts on isolated rat ventricular myocyte contraction. Coronary effluent collected during brief moderate hypoxia significantly depressed myocyte twitch shortening and decreased diastolic length, with only minor reduction in intracellular Ca2+ transients. These effects were similar to those of hypoxic rat cor

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DOUGHERTY, Christopher J., Lori A. KUBASIAK, Howard PRENTICE, Peter ANDREKA, Nanette H. BISHOPRIC, and Keith A. WEBSTER. "Activation of c-Jun N-terminal kinase promotes survival of cardiac myocytes after oxidative stress." Biochemical Journal 362, no. 3 (2002): 561–71. http://dx.doi.org/10.1042/bj3620561.

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Reperfusion injury occurs when ischaemic tissue is reperfused. It involves the generation and release of reactive oxygen that activates numerous signalling pathways and initiates cell death. Exposure of isolated cardiac myocytes to chronic hypoxia followed by reoxygenation results in the early activation of c-Jun N-terminal kinase (JNK) and death by apoptosis of approx. 30% of the myocytes. Although JNK activation has been described in a number of models of ischaemia/reperfusion, the contribution of JNK activation to cell fate has not been established. Here we report that the activation of JNK

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Sedmera, David, Pavel Kucera, and Eric Raddatz. "Developmental changes in cardiac recovery from anoxia-reoxygenation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 2 (2002): R379—R388. http://dx.doi.org/10.1152/ajpregu.00534.2001.

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The developing cardiovascular system is known to operate normally in a hypoxic environment. However, the functional and ultrastructural recovery of embryonic/fetal hearts subjected to anoxia lasting as long as hypoxia/ischemia performed in adult animal models remains to be investigated. Isolated spontaneously beating hearts from Hamburger-Hamilton developmental stages 14( 14HH), 20HH, 24HH, and 27HH chick embryos were subjected in vitro to 30 or 60 min of anoxia followed by 60 min of reoxygenation. Morphological alterations and apoptosis were assessed histologically and by transmission electro

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McKean, T., A. Scherzer, and H. Park. "Hypoxia and ischaemia in buffer-perfused toad hearts." Journal of Experimental Biology 200, no. 19 (1997): 2575–81. http://dx.doi.org/10.1242/jeb.200.19.2575.

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Previous studies on the effects of ischaemia or hypoxia in ectothermic vertebrate hearts have generally used preparations that were not performing at physiological levels of pressure and flow. The conclusions that ischaemia or hypoxia are not stressful to these organisms were examined in another species, Bufo marinus, in which a buffer-perfused heart was performing physiological levels of work. The in situ preparation demonstrated the Frank-Starling relationship and mechanical characteristics similar to the hearts of intact animals. The hearts recovered from 60 min of ischaemia and reperfusion

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Song, Jong Wook, Hyo Jung Kim, Hyelin Lee, Jae-woo Kim та Young-Lan Kwak. "Protective Effect of Peroxisome Proliferator-Activated ReceptorαActivation against Cardiac Ischemia-Reperfusion Injury Is Related to Upregulation of Uncoupling Protein-3". Oxidative Medicine and Cellular Longevity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/3539649.

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Activation of peroxisome proliferator-activated receptorα(PPARα) confers cardioprotection, while its mechanism remains elusive. We investigated the protective effect of PPARαactivation against cardiac ischemia-reperfusion injury in terms of the expression of uncoupling protein (UCP). Myocardial infarct size and UCP expression were measured in rats treated with WY-14643 20 mg/kg, a PPARαligand, or vehicle. WY-14643 increased UCP3 expressionin vivo. Myocardial infarct size was decreased in the WY-14643 group (76 ± 8% versus 42 ± 12%,P<0.05). During reperfusion, the incidence of arrhythmia was

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Parente, Valeria, Serena Balasso, Giulio Pompilio, et al. "Hypoxia/Reoxygenation Cardiac Injury and Regeneration in Zebrafish Adult Heart." PLoS ONE 8, no. 1 (2013): e53748. http://dx.doi.org/10.1371/journal.pone.0053748.

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Solevåg, A. L., G. M. Schmölzer, and P. Y. Cheung. "Hypoxia – Reoxygenation in neonatal cardiac arrest: Results from experimental models." Seminars in Fetal and Neonatal Medicine 25, no. 2 (2020): 101085. http://dx.doi.org/10.1016/j.siny.2020.101085.

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Baccaro, Cecilia, F. Bennardini, Germana Dini, et al. "Cardiac hypoxia and subsequent reoxygenation: sensitivity to L-arginine methylester." British Journal of Pharmacology 87, no. 4 (1986): 649–56. http://dx.doi.org/10.1111/j.1476-5381.1986.tb14581.x.

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Hasinoff, Brian B. "Dexrazoxane (ICRF-187) Protects Cardiac Myocytes Against Hypoxia-Reoxygenation Damage." Cardiovascular Toxicology 2, no. 2 (2002): 111–18. http://dx.doi.org/10.1385/ct:2:2:111.

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Prentice, H. M., I. A. Moench, Z. T. Rickaway, C. J. Dougherty, K. A. Webster, and H. Weissbach. "MsrA protects cardiac myocytes against hypoxia/reoxygenation induced cell death." Biochemical and Biophysical Research Communications 366, no. 3 (2008): 775–78. http://dx.doi.org/10.1016/j.bbrc.2007.12.043.

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Pearson, James T. "Cardiac responses to hypoxia and reoxygenation in Drosophila. New insights into evolutionarily conserved gene responses. Focus on “Cardiac responses to hypoxia and reoxygenation inDrosophila”." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 11 (2015): R1344—R1346. http://dx.doi.org/10.1152/ajpregu.00419.2015.

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Cunningham, M. J., C. S. Apstein, E. O. Weinberg, and B. H. Lorell. "Deleterious effect of ouabain on myocardial function during hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 3 (1989): H681—H687. http://dx.doi.org/10.1152/ajpheart.1989.256.3.h681.

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The effect of cardiac glycosides on myocardial function during hypoxia is controversial. Accordingly, we studied left ventricular performance during hypoxia and reoxygenation in the presence of a mildly inotropic, nontoxic dose of ouabain using isolated, isovolumic, buffer-perfused rabbit hearts. After 15 min of hypoxia, left ventricular developed pressure was less in the ouabain-treated group than in controls (35 +/- 4 vs. 55 +/- 3 mmHg, P less than 0.025). Left ventricular end-diastolic pressure (LVEDP) increased more during hypoxia in the presence of ouabain (9 +/- 1 to 32 +/- 7 with ouabai

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Funcke, Sandra, Tessa R. Werner, Marc Hein, et al. "Effects of the Delta Opioid Receptor Agonist DADLE in a Novel Hypoxia-Reoxygenation Model on Human and Rat-Engineered Heart Tissue: A Pilot Study." Biomolecules 10, no. 9 (2020): 1309. http://dx.doi.org/10.3390/biom10091309.

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Intermittent hypoxia and various pharmacological compounds protect the heart from ischemia reperfusion injury in experimental approaches, but the translation into clinical trials has largely failed. One reason may lie in species differences and the lack of suitable human in vitro models to test for ischemia/reperfusion. We aimed to develop a novel hypoxia-reoxygenation model based on three-dimensional, spontaneously beating and work performing engineered heart tissue (EHT) from rat and human cardiomyocytes. Contractile force, the most important cardiac performance parameter, served as an integ

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Zeng, Chao, Hu Li, Zhiwen Fan, et al. "Crocin-Elicited Autophagy Rescues Myocardial Ischemia/Reperfusion Injury via Paradoxical Mechanisms." American Journal of Chinese Medicine 44, no. 03 (2016): 515–30. http://dx.doi.org/10.1142/s0192415x16500282.

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Crocin, the main effective component of saffron, exerts protective effects against ischemia/reperfusion injury during strokes. However, the effects of crocin in myocardial ischemia/reperfusion injury, and the mechanisms involved, remain unknown. Pretreated with crocin for 7 days, C57BL/6N mice were subjected to 30 min of myocardial ischemia followed by 12[Formula: see text]h of reperfusion (for cardiac function and infarct size, cell apoptosis and necrosis). Neonatal mouse cardiomyocytes were subjected to 2 h of hypoxia followed by 4 h of reoxygenation. NMCM’s survival was assessed during hypo

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Thu, Vu Thi, Ngo Thi Hai Yen, and Nguyen Thi Ha Ly. "Liquiritin from Radix Glycyrrhizae Protects Cardiac Mitochondria from Hypoxia/Reoxygenation Damage." Journal of Analytical Methods in Chemistry 2021 (August 6, 2021): 1–11. http://dx.doi.org/10.1155/2021/1857464.

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Aims. The purpose of this study was to evaluate the protective effect of liquiritin (LIQ) from Radix Glycyrrhizae on cardiac mitochondria against hypoxia/reoxygenation (HR) injury. Methods. H9C2 cells were subject to the HR model. LIQ purified from Radix Glycyrrhizae (purity > 95%) was administrated to reoxygenation period. Cell viability, mitochondrial mass, mitochondrial membrane potential, reactive oxygen species, and mitochondrial Ca2⁺ level were then assessed by using Cell Counting kit-8 and suitable fluorescence probe kits. Results. LIQ administration remarkably reduced the rate of HR

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Shanmuganathan, Selvaraj, Derek J. Hausenloy, Michael R. Duchen, and Derek M. Yellon. "Mitochondrial permeability transition pore as a target for cardioprotection in the human heart." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (2005): H237—H242. http://dx.doi.org/10.1152/ajpheart.01192.2004.

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After an episode of myocardial ischemia, opening of the mitochondrial permeability transition pore (mPTP), at the onset of reperfusion, is a critical determinant of myocyte death. We investigated the role of the mPTP as a target for cardioprotection in the human heart. We subjected human atrial tissue, harvested from patients undergoing cardiac surgery, to a period of lethal hypoxia and investigated the effect of suppressing mPTP opening at the onset of reoxygenation. We found that suppressing mPTP opening at the onset of reoxygenation with known mPTP inhibitors cyclosporin A (CsA, 0.2 μmol/l)

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Liu, Yanan, Mark Paterson, Shelley L. Baumgardt, et al. "Vascular endothelial growth factor regulation of endothelial nitric oxide synthase phosphorylation is involved in isoflurane cardiac preconditioning." Cardiovascular Research 115, no. 1 (2018): 168–78. http://dx.doi.org/10.1093/cvr/cvy157.

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Abstract Aims Previous studies indicate that nitric oxide derived from endothelial nitric oxide synthase (eNOS) serves as both trigger and mediator in anaesthetic cardiac preconditioning. The mechanisms underlying regulation of eNOS by volatile anaesthetics have not been fully understood. Therefore, this study examined the role of vascular endothelial growth factor (VEGF) in isoflurane cardiac preconditioning. Methods and results Wistar rats underwent 30 min of coronary artery occlusion followed by 2 h of reperfusion. Isoflurane given prior to ischaemia/reperfusion significantly decreased myoc

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Korge, Paavo, Peipei Ping, and James N. Weiss. "Reactive Oxygen Species Production in Energized Cardiac Mitochondria During Hypoxia/Reoxygenation." Circulation Research 103, no. 8 (2008): 873–80. http://dx.doi.org/10.1161/circresaha.108.180869.

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Bordoni, Alessandra, Silvana Hrelia, Cristina Angeloni, et al. "Green tea protection of hypoxia/reoxygenation injury in cultured cardiac cells." Journal of Nutritional Biochemistry 13, no. 2 (2002): 103–11. http://dx.doi.org/10.1016/s0955-2863(01)00203-0.

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DUAN, J., and M. KARMAZYN. "Comparative responses of interfibrillar and subsarcolemmal cardiac mitochondria to hypoxia/reoxygenation*." Journal of Molecular and Cellular Cardiology 18 (1986): 23. http://dx.doi.org/10.1016/s0022-2828(86)80098-0.

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KIRSHENBAUM, L., M. HILL, and P. SINGAL. "Endogenous antioxidants in isolated hypertrophied cardiac myocytes and hypoxia-reoxygenation injury." Journal of Molecular and Cellular Cardiology 27, no. 1 (1995): 263–72. http://dx.doi.org/10.1016/s0022-2828(08)80025-9.

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Lodovici, Maura, Piero Dolara, Sandra Amerini, et al. "Effects of GM1 ganglioside on cardiac function following experimental hypoxia-reoxygenation." European Journal of Pharmacology 243, no. 3 (1993): 255–63. http://dx.doi.org/10.1016/0014-2999(93)90183-i.

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Hernandez, Olga M., Daryl J. Discher, Nanette H. Bishopric, and Keith A. Webster. "Rapid Activation of Neutral Sphingomyelinase by Hypoxia-Reoxygenation of Cardiac Myocytes." Circulation Research 86, no. 2 (2000): 198–204. http://dx.doi.org/10.1161/01.res.86.2.198.

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Dong, Ying-Ying, Min Wu, Anthony P. C. Yim, and Guo-Wei He. "Effect of Hypoxia-Reoxygenation on Endothelial Function in Porcine Cardiac Microveins." Annals of Thoracic Surgery 81, no. 5 (2006): 1708–14. http://dx.doi.org/10.1016/j.athoracsur.2005.12.002.

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Seko, Yoshinori, Kazuyuki Tobe, Naoyuki Takahashi, Yasushi Kaburagi, Takashi Kadowaki, and Yoshio Yazaki. "Hypoxia and Hypoxia/Reoxygenation Activate Src Family Tyrosine Kinases and p21rasin Cultured Rat Cardiac Myocytes." Biochemical and Biophysical Research Communications 226, no. 2 (1996): 530–35. http://dx.doi.org/10.1006/bbrc.1996.1389.

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Zhou, Yanqiong, Ganggang Shi, Jinhong Zheng, et al. "The protective effects of Egr-1 antisense oligodeoxyribonucleotide on cardiac microvascular endothelial injury induced by hypoxia–reoxygenationThis paper is one of a selection of papers published in this special issue entitled “Second International Symposium on Recent Advances in Basic, Clinical, and Social Medicine” and has undergone the Journal's usual peer review process." Biochemistry and Cell Biology 88, no. 4 (2010): 687–95. http://dx.doi.org/10.1139/o10-021.

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Early growth response 1 (Egr-1) over-expression has been demonstrated in myocardial ischemia–reperfusion injury, which is closely associated with endothelial dysfunction. In the present study we investigated the expression of Egr-1 on cultured cardiac microvascular endothelial cells (CMECs) to help define the mechanism of myocardial ischemia–reperfusion injury. A model of cultured CMECs exposed to hypoxia–reoxygenation was developed in which synthesized Egr-1 sense and antisense oligodeoxyribonucleotide were transfected into the cells. The expression of Egr-1 was examined by Western blot analy

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Shah, A. M., H. S. Silverman, E. J. Griffiths, H. A. Spurgeon, and E. G. Lakatta. "cGMP prevents delayed relaxation at reoxygenation after brief hypoxia in isolated cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 6 (1995): H2396—H2204. http://dx.doi.org/10.1152/ajpheart.1995.268.6.h2396.

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Previous studies in isolated cardiac myocytes suggest that impaired relaxation during reoxygenation after brief hypoxia results from abnormal Ca(2+)-myofilament interaction. Recent studies indicate that guanosine 3',5'-cyclic monophosphate (cGMP)-elevating interventions selectively enhance myocardial relaxation. We investigated the effect of 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) on posthypoxic relaxation in single rat myocytes, with simultaneous measurement of contraction and intracellular Ca2+ (indo 1 fluorescence). In control myocytes (n = 11), reoxygenation after 10 min of

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Robin, Elodie, Fabrice Marcillac, and Eric Raddatz. "A hypoxic episode during cardiogenesis downregulates the adenosinergic system and alters the myocardial anoxic tolerance." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 7 (2015): R614—R626. http://dx.doi.org/10.1152/ajpregu.00423.2014.

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To what extent hypoxia alters the adenosine (ADO) system and impacts on cardiac function during embryogenesis is not known. Ectonucleoside triphosphate diphosphohydrolase (CD39), ecto-5′-nucleotidase (CD73), adenosine kinase (AdK), adenosine deaminase (ADA), equilibrative (ENT1,3,4), and concentrative (CNT3) transporters and ADO receptors A1, A2A, A2B, and A3 constitute the adenosinergic system. During the first 4 days of development chick embryos were exposed in ovo to normoxia followed or not followed by 6 h hypoxia. ADO and glycogen content and mRNA expression of the genes were determined i

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Yamashita, N., M. Nishida, S. Hoshida, et al. "Alpha 1-adrenergic stimulation induces cardiac tolerance to hypoxia via induction and activation of Mn-SOD." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 4 (1996): H1356—H1362. http://dx.doi.org/10.1152/ajpheart.1996.271.4.h1356.

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We examined whether or not alpha 1-adrenergic stimulation increases the tolerance of the heart to ischemia using a hypoxia-reoxygenation model of cardiac myocytes. After exposure to norepinephrine (NE; 0.2 microM) for 24 h, the manganese superoxide dismutase (Mn-SOD) content and activity in the cells were increased from 0.61 +/- 0.03 to 0.87 +/- 0.04 microgram/dish and 22 +/- 1 to 55 +/- 4 U/dish, respectively. The specific activity of Mn-SOD was also increased from 36 to 63 U/microgram Mn-SOD protein after the stimulation with NE. Prazosin (2 microM) abolished the increase in Mn-SOD activity

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Stice, James P., Le Chen, Se-Chan Kim та ін. "17β-Estradiol, Aging, Inflammation, and the Stress Response in the Female Heart". Endocrinology 152, № 4 (2011): 1589–98. http://dx.doi.org/10.1210/en.2010-0627.

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Abstract Heat shock proteins (HSPs) are a cardioprotective class of proteins induced by stress and regulated by the transcription factor, heat shock factor (HSF)-1. 17β-estradiol (E2) indirectly regulates HSP expression through rapid activation of nuclear factor-κB (NF-κB) and HSF-1 and protects against hypoxia. As males experience a loss of protective cellular responses in aging, we hypothesized that aged menopausal (old ovariectomized) rats would have an impaired HSP response, which could be prevented by immediate in vivo E2 replacement. After measuring cardiac function in vivo, cardiac myoc

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MacCormack, Tyson J., and William R. Driedzic. "Mitochondrial ATP-sensitive K+ channels influence force development and anoxic contractility in a flatfish, yellowtail flounderLimanda ferruginea, but not Atlantic codGadus morhuaheart." Journal of Experimental Biology 205, no. 10 (2002): 1411–18. http://dx.doi.org/10.1242/jeb.205.10.1411.

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SUMMARYThe influence of ATP-sensitive K+ channels (KATPchannels) on cardiac performance during anoxia and reoxygenation was investigated in two species of fish showing different cardiac responses to anoxia. Force production in isometrically contracting ventricular muscle preparations from yellowtail flounder is potentiated at the onset of anoxia,while force immediately declines in Atlantic cod preparations. Glibenclamide,a general KATP blocker, impaired oxygenated force development in yellowtail flounder heart but was without effect on cod preparations. The mitochondrial KATP (mKATP)-specific

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