Alteration in calcium metabolism in mitochondria isolated from ischemic and reperfused myocardium.

C F Peng, M L Murphy, J J Kane, K D Straub
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Abstract

This study determines the effect of ischemia and reperfusion on energy-linked Ca2+ uptake by myocardial mitochondria. The left anterior descending coronary artery was occluded in 14 mature pigs for 2 hr. In seven animals the ligature was released and the ischemic zone reperfused for 2 additional hours. After sacrifice, mitochondrial function was measured in normal and reperfused or ischemic areas of the left ventricle, using a polarographic method. Mitochondria were prepared without EDTA by standard procedures and Ca2+ uptake measured by 45Ca2+ isotope tracer. Uptake of Ca2+ by mitochondria derived from ischemic myocardium is markedly impaired with or without phosphate. Reperfusion may accentuate this impairment. The presence of exogenous Ca2+ inhibits the ability of ischemic or reperfused mitochondria to phosphorylate ADP.

缺血心肌和再灌注心肌线粒体钙代谢的改变。
本研究确定缺血和再灌注对心肌线粒体能量相关Ca2+摄取的影响。14头成年猪左冠状动脉前降支闭塞2小时。7只动物解除结扎,缺血区再灌注2小时。牺牲后,用极谱法测定左心室正常区、再灌注区或缺血区线粒体功能。通过标准程序制备不含EDTA的线粒体,并通过45Ca2+同位素示踪剂测量Ca2+摄取。来自缺血心肌的线粒体对Ca2+的摄取在有或没有磷酸盐的情况下明显受损。再灌注可加重这种损伤。外源Ca2+的存在抑制了缺血或再灌注线粒体磷酸化ADP的能力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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