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Amiloride和耗竭细胞内糖原对心肌缺血再灌注损伤的影响

赵廷存, 张秀玲, 时安云, 徐海

(新乡医学院病理生理教研室，河南 新乡453003)；(北京医科大学病理生理教研室，北京100083)

摘要

本工作在离体大鼠等容收缩心脏模型上，观察在缺血前给予amiloride和耗竭心肌细胞内糖原以减少Na+-H+交换的底物对缺血后再灌注损伤的影响，以探讨Na+-H十交换和Na+-Caz+交换机制在心肌缺血后再灌注损伤中的发病学意义.结果表明，Amiloride及耗竭心肌细胞内糖原均能提高心脏血液动力学的恢复，心肌组织乳酸脱氢酶((LDH)漏出及丙二醛(MDA)生成减少，线粒体中谷胧甘肤过氧化物酶有较高的活性，心肌细胞内Na+, Ca2+超负荷减轻。Amiloride的心肌保护作用可能与其抑制再灌注初期的细胞膜Na+-H+交换机制有关。耗竭细胞内糖原因减少缺血末细胞内H+的堆积，使Na+-H十交换底物减少而抑制Na+-H+交换机制。

关键词： amiioride; 耗竭糖原; 再灌注损伤; Na~(+)H~(+)十交换; Na~(+)-Ca~(2+)交换

EFFECTS OF AMILORIDE AND GLYCOGEN DEPLETION ON POST-ISCHEIV耳C REPERFUSION INJURY OF ISOVOLUMIC PERFUSED RAT HEARTS

Zhao Tingcun, Zhang Xiuling, Shi Anyun, Xu Hai

(Department of Pathorphysiology Xinximcg Medical College, Xinxiang 453003)；(DWtmed of Pathophysiology, Beijing Mediatl University, Beijing 100083)

Abstract

The efftcts of amiloride (0. 5 nmol/L) and glycogen depletion were studied to find out the possible roles of Na+-H+ exchange of ischemia reperfusion injury in the isovolumic perfused isolated rat hearts. The data indicated that, compared to control group，both amiloride and glycogen depletion accelerated recovery of hemodynamics and reduced leakage of LDH and the formation of myocardial MDA which was accompared by a higher activity of mitochondrial GSH-Px and lesser accumlation of intracellular Na+，Cal+. That Na+-H+ and Na+-Cal+ exchanges might play a critical role in postischemic reperfusion injury is discussed.

Key words: Key words:amiloride;reperfusion injury;Na~(+)-Ca~(2+ )exchange ;;

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引用本文：

赵廷存, 张秀玲, 时安云, 徐海. Amiloride和耗竭细胞内糖原对心肌缺血再灌注损伤的影响[J]. 生理学报 1996; 48 (2): .

Zhao Tingcun, Zhang Xiuling, Shi Anyun, Xu Hai. EFFECTS OF AMILORIDE AND GLYCOGEN DEPLETION ON POST-ISCHEIV耳C REPERFUSION INJURY OF ISOVOLUMIC PERFUSED RAT HEARTS. Acta Physiol Sin 1996; 48 (2): (in Chinese with English abstract).