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目的探讨脑外伤和伴发低血压的脑外伤对于大鼠脑水肿形成时间和程度的影响。方法利用组织比重法测定创伤后大鼠顶叶皮层和纹状体含水量的变化。通过联合使用氯醛糖和潘龙诱发脑外伤后低血压。结果改良的加速性脑创伤模型大鼠病死率为48．6%,而颅骨骨折的发生率为6．4%。创伤后8 h和24 h存活大鼠,其脑组织含水量与对照组比较无明显差别；但创伤后24 h较8 h大鼠,其顶叶皮层含水量[(79．1±0．5)%vs．(78．6±0．5)%,P＜0．05]增加0．5%。然而,创伤后合并低血压大鼠,创伤后8 h就已出现明显的脑水肿。与创伤后8 h存活大鼠相比,其顶叶皮层含水量[(81．5±0．9)%vs．(78．6±0．5)%,P＜0．01]和纹状体含水量[(78．5±0．9)%vs．(75．5±0．9)%,P＜0．01]均明显增加,即,创伤后合并低血压使大鼠脑组织含水量增加了2．9%。结论无低血压的颅脑外伤大鼠,其脑水肿形成晚且程度轻；而合并有低血压的脑外伤大鼠,其脑水肿出现早且严重。
Objective To investigate the effect of traumatic brain injury (TBI) and traumatic brain injury associated with hypotension on the time and extent of brain edema in rats. Methods The changes of water content in the parietal cortex and striatum of traumatized rats were determined by tissue gravimetric method. Hypotension after traumatic brain injury is induced by the combination of chloralose and pandion. Results The improved model of accelerated traumatic brain injury in rats was 48.6%, while the incidence of skull fractures was 6.4%. There was no significant difference in the brain water content between the rats survived 8 h and 24 h after trauma compared with the control group. However, the water content of the parietal cortex in the rats at 24 h after trauma was (79.1 ± 0.5 % vs. (78.6 ± 0.5)%, P <0.05] increased by 0.5%. However, post-traumatic hypotension rats developed obvious brain edema at 8 h post-trauma. The parietal cortex water content was (81.5 ± 0.9)% vs that of the surviving rats at 8 h after trauma. (78.6 ± 0.5)%, P <0.01] and striatum water content [(78.5 ± 0.9)% vs. (75.5 ± 0.9)%, P <0.01]. In other words, the water content in rat brain increased 2.9% after trauma combined with hypotension. Conclusions Brain edema in rats with hypothalamic traumatic brain injury is late and mild. However, cerebral edema in rats with hypotension is earlier and more severe.