Cardioprotective Effects of MET-88, a Gamma-Butyrobetaine Hydroxylase Inhibitor, on Cardiac Dysfunction Induced by Ischemia/Reperfusion in Isolated Rat Hearts

Pharmacology ◽  
2000 ◽  
Vol 61 (4) ◽  
pp. 238-243 ◽  
Author(s):  
Yukio Hayashi ◽  
Kiyotaka Tajima ◽  
Tsukasa Kirimoto ◽  
Hidekazu Miyake ◽  
Naosuke Matsuura
Keyword(s):  
Cardiac Dysfunction ◽  
Ischemia Reperfusion ◽  
Rat Hearts ◽  
Cardioprotective Effects ◽  
Isolated Rat

scholarly journals Molecular hydrogen potentiates beneficial anti-infarct effect of hypoxic postconditioning in isolated rat hearts: a novel cardioprotective intervention

2017 ◽  
Vol 95 (8) ◽  
pp. 888-893 ◽  
Author(s):  
Marek Zálešák ◽  
Branislav Kura ◽  
Ján Graban ◽  
Veronika Farkašová ◽  
Ján Slezák ◽  
...  
Keyword(s):  
Molecular Hydrogen ◽  
Redox Reactions ◽  
Heart Function ◽  
Ischemia Reperfusion ◽  
Area At Risk ◽  
Rat Hearts ◽  
Hypoxic Postconditioning ◽  
Cardioprotective Effects ◽  
Krebs Henseleit Buffer ◽  
Isolated Rat

Generation of free radicals through incomplete reduction of oxygen during ischemia–reperfusion (I/R) is well described. On the other hand, molecular hydrogen (H2) reduces oxidative stress due to its ability to react with strong oxidants and easily penetrate cells by diffusion, without disturbing metabolic redox reactions. This study was designed to explore cardioprotective potential of hypoxic postconditioning (HpostC) against I/R (30 min global I – 120 min R) in isolated rat hearts using oxygen-free Krebs-Henseleit buffer (KHB). Furthermore, the possibility to potentiate the effect of HpostC by H2using oxygen-free KHB saturated with H2(H2+ HpostC) was tested. HPostC was induced by 4 cycles of 1-minute perfusion with oxygen-free KHB intercepted by 1-minute perfusion with normal KHB, at the onset of reperfusion. H2+ HPostC was applied in a similar manner using H2-enriched oxygen-free KHB. Cardioprotective effects were evaluated on the basis of infarct size (IS, in % of area at risk, AR) reduction, post-I/R recovery of heart function, and occurrence of reperfusion arrhythmias. HPostC significantly reduced IS/AR compared with non-conditioned controls. H2present in KHB during HPostC further decreased IS/AR compared with the effect of HPostC, attenuated severe arrhythmias, and significantly restored heart function (vs. controls). Cardioprotection by HpostC can be augmented by molecular hydrogen infusion.

scholarly journals Determination of Oxidative Stress and Cardiac Dysfunction after Ischemia/Reperfusion Injury in Isolated Rat Hearts

2013 ◽  
Vol 19 (3) ◽  
pp. 186-194 ◽  
Author(s):  
Hitoshi Inafuku ◽  
Yukio Kuniyoshi ◽  
Satoshi Yamashiro ◽  
Katsuya Arakaki ◽  
Takaaki Nagano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Cardiac Dysfunction ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Hearts ◽  
Isolated Rat

scholarly journals Involvement of γ-Glutamyl Transpeptidase in Ischemia/Reperfusion-Induced Cardiac Dysfunction in Isolated Rat Hearts

2019 ◽  
Vol 42 (11) ◽  
pp. 1947-1952 ◽  
Author(s):  
Takeshi Koyama ◽  
Akari Tsubota ◽  
Tatsuya Sawano ◽  
Masashi Tawa ◽  
Bunta Watanabe ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Ischemia Reperfusion ◽  
Rat Hearts ◽  
Glutamyl Transpeptidase ◽  
Isolated Rat

scholarly journals Attenuation of extracellular ATP response in cardiomyocytes isolated from hearts subjected to ischemia-reperfusion

2005 ◽  
Vol 289 (2) ◽  
pp. H614-H623 ◽  
Author(s):  
Harjot K. Saini ◽  
Vijayan Elimban ◽  
Naranjan S. Dhalla
Keyword(s):  
Cardiac Function ◽  
Positive Inotropic Effect ◽  
Ischemia Reperfusion ◽  
Cardiac Contractility ◽  
Extracellular Atp ◽  
Binding Characteristics ◽  
Rat Hearts ◽  
The Status ◽  
Intracellular Ca ◽  
Isolated Rat

Extracellular ATP is known to augment cardiac contractility by increasing intracellular Ca2+ concentration ([Ca2+]i) in cardiomyocytes; however, the status of ATP-mediated Ca2+ mobilization in hearts undergoing ischemia-reperfusion (I/R) has not been examined previously. In this study, therefore, isolated rat hearts were subjected to 10–30 min of global ischemia and 30 min of reperfusion, and the effect of extracellular ATP on [Ca2+]i was measured in purified cardiomyocytes by fura-2 microfluorometry. Reperfusion for 30 min of 20-min ischemic hearts, unlike 10-min ischemic hearts, revealed a partial depression in cardiac function and ATP-induced increase in [Ca2+]i; no changes in basal [Ca2+]i were evident in 10- or 20-min I/R preparations. On the other hand, reperfusion of 30-min ischemic hearts for 5, 15, or 30 min showed a marked depression in both cardiac function and ATP-induced increase in [Ca2+]i and a dramatic increase in basal [Ca2+]i. The positive inotropic effect of extracellular ATP was attenuated, and the maximal binding characteristics of 35S-labeled adenosine 5′-[γ-thio]triphosphate with crude membranes from hearts undergoing I/R was decreased. ATP-induced increase in [Ca2+]i in cardiomyocytes was depressed by verapamil and Cibacron Blue in both control and I/R hearts; however, this response in I/R hearts, unlike control hearts, was not affected by ryanodine. I/R-induced alterations in cardiac function and ATP-induced increase in [Ca2+]i were attenuated by treatment with an antioxidant mixture and by ischemic preconditioning. The observed changes due to I/R were simulated in hearts perfused with H2O2. The results suggest an impairment of extracellular ATP-induced Ca2+ mobilization in I/R hearts, and this defect appears to be mediated through oxidative stress.

Effect of cicletanine on ischemia/reperfusion-induced ion shifts in isolated rat hearts

1990 ◽  
Vol 22 ◽  
pp. S64
Author(s):  
Arpad Tosaki ◽  
Matyas Koltai ◽  
Thierry Tarrade ◽  
Pierre Braquet
Keyword(s):  
Ischemia Reperfusion ◽  
Rat Hearts ◽  
Ion Shifts ◽  
Isolated Rat
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