Effect of ischemic preconditioning on mitochondrial oxidative phosphorylation and high energy phosphates in rat hearts
Effect of ischemic preconditioning on mitochondrial oxidative phosphorylation and high energy phosphates in rat hearts
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DOI：
10.1006/jmcc.1996.0038
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发表时间：
1996-02-01
影响因子：
5
通讯作者：
Nakagawa, M
中科院分区：
文献类型：
--
作者：
Kobara, M;Tatsumi, T;Nakagawa, M
缺血预处理（IP）保护心肌免受长时间缺血的能力可能来自于改善能量平衡。因此，我们研究了心肌能量代谢和线粒体氧化磷酸化在离体灌注大鼠心脏，无论是受到（IP组），或不受（对照组），预处理前30分钟持续缺血和30分钟再灌注。预处理是通过两个循环的5分钟缺血然后5分钟再灌注来实现的。IP组的心肌功能恢复明显更好，肌酸激酶释放明显更低。虽然ATP水解在持续缺血期间在两组中保持不变，但高能磷酸盐（例如，IP组在再灌注后观察到ATP和CP。预处理后即刻的CP含量大大超过缺血前的值。IP组持续缺血时乳酸产生明显减少，提示无氧糖酵解减少，细胞内酸中毒可能减轻。对照组持续缺血和再灌注后寡霉素敏感性线粒体ATP酶活性均明显降低，但IP组在预处理、持续缺血和再灌注后均无变化。缺血再灌注后，两组线粒体ATP酶活性均明显降低，但IP组再灌注后活性明显升高。提示：（1）线粒体ATP酶对缺血再灌注时ATP消耗的贡献很小;（2）CP过冲现象和无氧糖酵解减少均可能是持续性缺血时的心肌保护作用，ATP酶和腺苷酸转位酶活性的保存可能是心肌缺血再灌注损伤后高能磷酸盐恢复的原因之一。(C)1996年学术出版社
The ability of ischemic preconditioning (IP) to protect the myocardium against prolonged ischemia may derive from improved energy balance. We therefore examined myocardial energy metabolism and mitochondrial oxidative phosphorylation in isolated perfused rat hearts which were either subjected (IP group), or not subjected (control group), to preconditioning prior to 30 min sustained ischemia and 30 min reperfusion. Preconditioning was achieved with two cycles of 5 min ischemia followed by 5 min reperfusion. Recovery of myocardial function was significantly greater, and creatine kinase release was significantly lower, in the IP group. Although ATP hydrolysis during the sustained ischemia remained unchanged in both groups, greater preservation of high energy phosphate (eg. ATP and CP) was observed in the IP group after reperfusion. CP content immediately after preconditioning greatly exceeded pre-ischemic values. Lactate production during the sustained ischemia was significantly lower in the IP group, suggesting a decrease in anaerobic glycolysis and a probable attenuation of intracellular acidosis, Oligomycin-sensitive mitochondrial ATPase activity in the control group was significantly decreased both after the sustained ischemia and the reperfusion, but in the IP group it did not change after the preconditioning, sustained ischemia, or reperfusion. Although atractyloside-inhibitable adenine nucleotide translocase activity was markedly decreased during sustained ischemia in both groups, its activity was significantly higher after reperfusion in the IP group, These data suggest that (1) mitochondrial ATPase contributes only slightly to ATP depletion during sustained ischemia, (2) both the CP overshoot phenomenon and the decrease in anaerobic glycolysis can be attributable to cardioprotection during the sustained ischemia, and (3) the preservation of ATPase and adenine nucleotide translocase activities may be a possible explanation for the restoration of high energy phosphates after sustained ischemia-reperfusion injury in the preconditioned hearts of rats. (C) 1996 Academic Press Limited