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Bibliographies thématiques / Cardiac hypoxia reoxygenation

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Littérature scientifique sur le sujet « Cardiac hypoxia reoxygenation »

Auteur : Grafiati

Publié le 10 mars 2023

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Articles de revues sur le sujet "Cardiac hypoxia reoxygenation"

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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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