急性心肌梗塞时心肌线粒体钙变化的实验研究

Changes of myocardial mitochondrial Ca^(2+)in acute myocardial infarction

用Ｖｉａｌ方法分离心肌线粒体，按Ｎａｋａｎｉｓｈｉ方法测定线粒体钙，并按张源鑫方法测定Ｃａ２＋－Ｍｇ２＋－ＡＴＰａｓｅ（钙－镁－三磷酸腺苷酶），研究心肌缺血后心肌线粒体钙变化，线粒体膜Ｃａ２＋－Ｍｇ２＋－ＡＴＰａｓｅ活性并相应观察心肌的超徽结构变化。结果表明缺血后心肌线粒体钙明显增高，缺血３０ｍｉｎ和正常组比较Ｐ＜０．０５，６０ｍｉｎ和１８０ｍｉｎ增高更明显。此变化和心肌线粒体超微结构改变相吻合，缺血３０ｍｉｎ时线粒体肿胀，此时尚为可逆性变化。６０、１８０ｍｉｎ后线粒体出现坏死。线粒体Ｃａ２＋－ＡＴＰａｓｅ在缺血后呈进行性下降（Ｐ＜０．０１。说明线粒体Ｃａ２＋－ＡＴＰａｓｅ活性降低是导致线粒体钙超载的原因之一。

The changes of mitochondrial Ca2+,activity of membraneous Ca2+-Mg2+-ATPase and myocardial ultrastucture were studied after myocardial ischemia in acute coronary artery occlusion.It was found that the mitochondrial Ca2+ was obviously elevated in 0.5 h after ischemia(vs the control,P<0.05 )and further elevated in 1 h and 3 h after ischema,which was in accordance with the changes of the myocardial mitochondria. The mitochondria swelled 30 min after ischemia ,which was still a reversible change. But they became necrotic in 60 min and 180 min after ischemia. The activity of mitochondrial membraneous Ca2+-ATPase was progressively declined after ischemia(vs the control,P<0.01).The findings suggest that the decline of the activity of Ca2+-ATPase is one of the cau see for overloading of the mitochondrial Ca2+.