1995
DOI: 10.1161/01.cir.91.11.2810
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Mechanisms of Ischemic Preconditioning in Rat Myocardium

Abstract: The results indicate that preconditioning causes inhibition of rat heart mitochondrial ATPase that persists during reperfusion so that the enzyme is inhibited from the very beginning of the sustained ischemia. This inhibition leads to sparing of high-energy phosphates and improves the time-averaged energy state during ischemia. Although a causal relationship is difficult to prove, this reversible inhibition may contribute to postischemic recovery of the heart.

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Cited by 119 publications
(44 citation statements)
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“…Similarly, oligomycin, which inhibits F 1 F o -ATPase through its F o domain, preserves ATP and protects against or postpones injury during ischemia (72). However, it is difficult to envisage how inhibition of mitochondrial F 1 F o -ATPase by dietary resveratrol and related polyphenols could have a similar effect and so contribute to the cardiovascular protective effects associated with dietary polyphenols.…”
Section: Mechanism Of Inhibitionmentioning
confidence: 99%
“…Similarly, oligomycin, which inhibits F 1 F o -ATPase through its F o domain, preserves ATP and protects against or postpones injury during ischemia (72). However, it is difficult to envisage how inhibition of mitochondrial F 1 F o -ATPase by dietary resveratrol and related polyphenols could have a similar effect and so contribute to the cardiovascular protective effects associated with dietary polyphenols.…”
Section: Mechanism Of Inhibitionmentioning
confidence: 99%
“…The binding pocket for the F1-targeting inhibitor efrapeptin is localized in a, b and g subunits while that for aurovertin B is localized mainly in the b subunit . Inhibition of F0F1-ATPase/ATP synthase by the F0-targeting inhibitor, oligomycin, has been shown to protect or postpone cell injury by preserving ATP during ischaemia (Vuorinen et al, 1995) and to induce apoptosis in tumour cells (Wolvetang et al, 1994). Oligomycin also inhibits the apoptosis induced by Bax, a pro-apoptotic protein localized on the mitochondrial outer membrane, and F0F1-ATPase is required for the killing of cells by Bax (Matsuyama et al, 1998).…”
Section: Introductionmentioning
confidence: 99%
“…Так была предложена метаболи-ческая концепция ишемического прекондициониро-вания. Полагают, что энергосберегающие эффекты ИП вызваны снижением активности протонной ми-тохондриальной F 0 F 1 АТФазы, дефосфорилирующей основное количество АТФ при ишемии [111]. На-ряду с этим снижается активность Na…”
Section: Aadsorasunclassified