【摘要】 本文通过犬急性心肌缺血－再灌注模型探讨缺血－再灌注心肌Ｃａ２＋超负荷的发生机制。当心肌持续缺血１５０ｍｉｎ，心肌细胞内Ｃａ２＋、Ｎａ＋增加、Ｋ＋降低；心肌细胞膜Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ、Ｃａ２＋－ＡＴＰａｓｅ活性降低，心肌组织丙二醛（ＭＤＡ）含量增加．而心肌缺血９０ｍｉｎ后，再灌注６０ｍｉｎ，与之比较细胞内Ｃａ２＋明显增加，伴Ｎａ＋升高、Ｋ＋降低，心肌细胞膜Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ、Ｃａ２＋－ＡＴＰａｓｅ活性降低，ＭＤＡ含量增加，说明缺血－再灌注过程中Ｎａ＋升高、Ｎａ＋－Ｃａ２＋交换增加，Ｃａ２＋－ＡＴＰａｓｅ活性降低是细胞内Ｃａ２＋超负荷发生的重要原因。更多还原

【Abstract】 The aim of this experiment is to study the mechanism of the Ca2+ -overloading in dog model during the process of ischemic reperfusion,As the myocardium sustained ischemia for 150 min,the intracellular Ca2+,Na+ were increased,K+ was decreased,the activity of myocardial sarcolemma Na+-K+ATP ase and Ca2+ ATP ase decreased,and the concentration of MDA increased.In ischemic reperfusion group in which myocardial ischemia was maintained for 90 min and subsequent reperfusion for 60 min,in comparison with the group of ischemia without reperfusion,the Ca2+of myocardial cells was increased remarkably,Na+increased and K+ decreased,the activity of Na+ -K+ -ATP ase and Ca2+ -ATPase decreased and the concentration of MDA increased. These data suggest that increased Na+-Ca2+ exchange,increase in Na+and decrease of the activity of Ca2+ATPase may be important causes of Ca2+-overloading in the course of ischemic reperfusion.更多还原