2009Acta Academiae Medicinae CPAFRequires access

Effects of SEA0400 on myocardial ischemia-reperfusion injury in isolated rat hearts

Chen Yang

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Abstract

【Objective】To study the cardioprotective effects and mechanisms of SEA0400 on myocardial ischemia-reperfusion injury in isolated rat hearts. 【Methods】Ischemia-reperfusion injury was induced by 40 min of global ischemia and 60 min of reperfusion in isolated rat hearts.Left ventricular developed pressure(LVDP) and the first derivative(±dp/dtmax) were recorded.Tissue ATP content, mitochondrial Ca2+ concentration(m) and mitochondrial membrane potential(ΔΨ) were measured.【Results】SEA0400 enhanced the recovery of contractile force and attenuated tissue ATP content decrease during ischemia-reperfusion.Ischemia-reperfusion resulted in the depolarization of the mitochondrial membrane potential and an increase in mitochondrial Ca2+ concentration,and SEA0400 significantly delayed these changes.【Conclusions】SEA0400 maintains mitochondrial function and tissue ATP content during ischemia through the inhibition mitochondrial Ca2+ overload

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【Objective】To study the cardioprotective effects and mechanisms of SEA0400 on myocardial ischemia-reperfusion injury in isolated rat hearts. 【Methods】Ischemia-reperfusion injury was induced by 40 min of global ischemia and 60 min of reperfusion in isolated rat hearts.Left ventricular developed pressure(LVDP) and the first derivative(±dp/dtmax) were recorded.Tissue ATP content, mitochondrial Ca2+ concentration(m) and mitochondrial membrane potential(ΔΨ) were measured.【Results】SEA0400 enhanced the recovery of contractile force and attenuated tissue ATP content decrease during ischemia-reperfusion.Ischemia-reperfusion resulted in the depolarization of the mitochondrial membrane potential and an increase in mitochondrial Ca2+ concentration,and SEA0400 significantly delayed these changes.【Conclusions】SEA0400 maintains mitochondrial function and tissue ATP content during ischemia through the inhibition mitochondrial Ca2+ overload

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Available abstract

【Objective】To study the cardioprotective effects and mechanisms of SEA0400 on myocardial ischemia-reperfusion injury in isolated rat hearts. 【Methods】Ischemia-reperfusion injury was induced by 40 min of global ischemia and 60 min of reperfusion in isolated rat hearts.Left ventricular developed pressure(LVDP) and the first derivative(±dp/dtmax) were recorded.Tissue ATP content, mitochondrial Ca2+ concentration(m) and mitochondrial membrane potential(ΔΨ) were measured.【Results】SEA0400 enhanced the recovery of contractile force and attenuated tissue ATP content decrease during ischemia-reperfusion.Ischemia-reperfusion resulted in the depolarization of the mitochondrial membrane potential and an increase in mitochondrial Ca2+ concentration,and SEA0400 significantly delayed these changes.【Conclusions】SEA0400 maintains mitochondrial function and tissue ATP content during ischemia through the inhibition mitochondrial Ca2+ overload

Key concepts: Ischemia, Reperfusion injury, Mitochondrion, Depolarization, Internal medicine, Cardiology, Myocardial ischemia, Membrane potential

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