Amiloride和耗竭细胞内糖原对心肌缺血再灌注损伤的影响

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＋交换和Ｎａ＋－Ｃａ２＋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，线粒体中谷胱甘肽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＋交换底物减少而抑制Ｎａ＋－Ｈ＋交换机制。

EFFECTS OF AMILORIDE AND GLYCOGEN DEPLETION ON POST-ISCHEMIC REPERFUSION INJURY OF ISOVOLUMIC PERFUSED RAT HEARTS

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 reper fusion 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 , Ca2 . That Na -H and Na -Ca2 exchanges might play a critical role in postischemic reperfusion injury is discussed.