局灶脑缺血后线粒体ATP酶的活性变化

The changes of mitochondrial ATPase activities after focal cerebral ischemia

应用兔大脑中动脉阻断（ＭＣＡＯ）模型，超速离心分离出脑细胞线粒体，生化法测其Ｎａ~＋，ｋ~＋－ＡＴＰ酶，Ｃａ^（２＋），Ｍｇ^（２＋）－ＡＴＰ酶活性，戊巴比妥酸荧光法测其丙二醛含量。结果发现脑缺血后线粒体丙二醛含量显著增加，且随缺血时间的延长而递增；线粒体ＡＴＰ酶（Ｎａ~＋，Ｋ~＋－ＡＴＰ酶、Ｃａ^（２＋），Ｍｇ^（２＋）－ＡＴＰ酶）活性则下降，且随缺血时间延长而递降；相关回归发现线粒体丙二醛含量与ＡＴＰ酶活性之间呈显著负相关。该结果提示脑缺血后线粒体ＡＴＰ酶活性变化参与脑缺血脑水肿的发生发展，其活性变化与自由基反应有关。

Abstract Using the rabbit model of middle cerebral artery occlusion we dissected the brain mitochondria of which Na￣+, K￣+-ATPase, Ca￣(2+),Mg￣(2+)-ATPase activities were determined by biochemical method and the contents of malondialdehyde (MDA) were measured by TBA method. We found that the activities of mitochondria ATPase were decreased after cerebral ischemia and these changed much more with the delay of ischemic time, but the contents of MDA changed oppositly.There were negative correlation between the activities of ATPase and the contents of MDA. These results suggested that the changes of mitochondrial ATPase activities took part in the development of ischemic brain edema and these changes might associate With the reaction of free radicals.