实验性颅脑损伤家兔线粒体Ca^(2+)-ATPase活性的变化

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

目的测定家兔急性外伤性脑水肿后，脑细胞线粒体Ca2＋－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Ca2＋－ATPase活性，MDA含量．结果：线粒体Ca2＋－ATPase活性在伤后4h即开始下降，至48h降到最低（P＜0．01），MDA含量显著增加，随时间延长增加更明显（P＞0．01），MDA与Ca2＋－ATPase之间呈负相关（r＝－0.885，P＜0．01），脑损伤后脑水含量增多，与Ca2＋－ATPase活性降低、MDA增高有关．结论：脑损伤后氧自由基大量产生，使Ca2＋－ATPase活性受到抑制，脑细胞线粒体Ca2＋－ATPase活性降低是继发性脑损伤发生和发展的重要因素之一．

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