实验性颅脑损伤家兔线粒体Ca^2＋—ATPase活性的变化

测定家兔急性外伤性脑水肿后，脑细胞线粒体Ｃａ＾２＋－ＡＴＰａｓｅ活性及ＭＤＡ含量，探讨其在继发性脑损伤中的作用。方法利用家兔自由落体损伤模型在伤后４，８，２４，４８ｈ测定脑细胞线粒体Ｃａ＾２＋－ＡＴＰａｓｅ活必一粒体Ｃａ＾２＋－ＡＴＰａｓｅ活性在伤后４ｈ即开始下降，至４８ｈ降到最低，ＭＤＡ含量显著增加，随时间延长增加更明显，ＭＤＡ与Ｃａ＾２＋－ＡＴＰａｓｅ之间呈负相关，脑损伤后脑水含量增多，与Ｃａ

The changes in Ca~(2+)-ATPase activities in rabbit mitochondria after experimental brain injury

objectivet:To determine the activities of Ca2+-ATPase and the contents of MDA in rabbit brain mitochondria after traumatic brain edema. Methods:Using rabbit model of skull impact the activities of Ca2+-ATPase and the contents of MDA were determined in 4,8.24,48h after injury. Results. Ca2+-ATPa-se activities in mitochondria decreased in 4h and minimized in 48h after injury(P<0.01). the contents of NDA increased significantly with much more changes with the delay of time (P<0.01). There was negative correlation between the activities of Ca2+-ATPase and thc contents of MDA(r=-0.885, P<0.01). These results suggest that the increase in brain water is associated with the changes in Ca2+-ATPase and MDA. Conclusions:Oxygen free radicals from brain injury inhibit the activities of Ca2+-ATPase. which is one of the important reasons for the occurrence and development of secondery brain injury