亚低温治疗对脑创伤后三磷酸腺苷酶的影响

目的 观察亚低温治疗对大鼠脑外伤后脑组织Na^ -K^ -ATP酶、Mg^2 -ATP酶以及Ca^ -ATP酶的影响。方法 75只大鼠随机分为常温对照组（33只）、常温受伤组（22只）和亚低温治疗组（20只），后两组用自由落体方法致大鼠左侧脑外伤，亚低温治疗组受伤后用冰袋全身降温至脑温30℃后维持1h，然后加热复温至37℃。每组大鼠在伤后3h,1,3,5和7d取大脑组织，测定组织匀浆液中ATP酶的活性。结果 （1）Na^ -K^ -ATP酶；常温受伤组和亚低温治疗组在3h明显高于对照组，而后明显下降。亚代温治疗组在第3天明显高于常温受伤组；（2)Mg^2 -ATP酶；常温受伤组和亚低温治疗组在1d后才开始明显下降，但亚低温治疗组在1d和3d中较常温组睛降速度明显变慢；（3）Ca^2 -ATP酶：常温受伤组第1天就较常温对照组明显下降，而亚低温治疗组3h和第1天保持正常，有3天才明显下降，但仍然显著高于常温受伤组。结论（1）脑外伤大鼠脑细胞Na^2 -K^ -ATP酶早期对脑外伤有应激反应，亚低温治疗对细胞钠通道的作用不明显；（2）亚低温对钙泵有明显的调节作用，较常温受伤组显著提高脑细胞Ca^2 -Mg^2 -ATP酶的活性；（3）亚低温治疗能延缓脑细胞钙通道的损伤时间，且在7d内脑细胞的钠通道和钙通道在低水平保持相对稳定，从而减少Ca^2 的内流，减轻脑水肿。

Effects of hypothermia on ATPase following brain trauma in rats

Objective　To investigate the effects of hypothermia on the contents of Na+-K+-ATPase, Mg2+-ATPase and Ca2+-ATPase in traumatic rats. 　Methods　 Seventy five Wistar rats were divided randomly into three groups : the non-traumatic control group (n=33), the normothermia traumatic group (n=22) and the hypothermia-treated group (n=20). Brain trauma was induced on the left cerebrum by free falling objects. The whole body of the animals in the hypothermia-treated group was cooled to 30℃ for 1 hour, then heated to 37℃. The cerebrum tissues were obtained at 3 hours, 1 day, 3 days, 5 days and 7 days, respectively, and ATPase activities of the tissues' homogenate were measured. 　Results　Compared with the control group, the activities of Na+-K+-ATPase in the normothermia traumatic group and in the hypothermia-treated group increased at 3 hours after trauma, then markedly decreased in the following days (P<0.01). And the activities of Na+-K+-ATPase in the hypothermia-treated group at 3 days were much higher than that in the normothermia traumatic group. The activities of Mg2+-ATPase in both of the normothermia traumatic group and the hypothermia-treated group significantly decreased after 24 hours compared with that of the normal controls, but the decreasing speed in the hypothermia-treated group at 1 day and 3 days was much lower than that in the normothermia traumatic group. The activities of Ca2+-ATPase in the normothermia traumatic group markedly decreased at 1 day compared with the normal controls, and they were kept in normality in the hypothermia-treated group until 3 days, which were still much higher than that of the normothermia traumatic group.　Conclusions　There is an irritable reaction of Na+-K+-ATPase activity in cerebrum tissues during the early period of brain trauma. Hypothermia has little effect on sodium pump. But hypothermia can evidently increase the activities of Ca2+-ATPase and Mg2+-ATPase compared with the normothermia, and it has a significant regulation on calcium pump. The sodium and calcium pump can be kept in stable situation at lower activities after hypothermia. Hypothermia treatment can delay the injury of cerebrum calcium pump and decrease the influx of calcium and cerebral edema.