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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。
In this paper, we explored the mechanism of Ca2 + overload induced by ischemia-reperfusion in canine model of acute myocardial ischemia-reperfusion. Myocardial cell membrane Na + -K + -ATPase, Ca2 + -ATPase activity decreased myocardial MDA content increased when myocardial ischemia continued for 150min, myocardial Ca2 +, Na + increased, K + decreased. The myocardial ischemia 90min, reperfusion 60min, compared with intracellular Ca2 + increased significantly, accompanied by increased Na +, K decreased, myocardial cell membrane Na + -K + -ATPase, Ca2 + -ATPase activity decreased MDA content, indicating that ischemia- During reperfusion Na + increases, Na + -Ca2 + exchange increases, Ca2 + -ATPase activity is an important cause of intracellular Ca2 + overload.