大鼠弥漫性颅脑损伤后脑水肿和病理学变化

目的探讨大鼠弥漫性颅脑损伤后病理学变化规律及意义。方法成年健康SD雄性大鼠100只，以自由落体法建立大鼠弥漫性颅脑损伤模型，随机平均分为对照组及外伤后1h、3h、6h、12h、24h、48h、72h、7d和14d等10组．检测大鼠脑组织含水量并观察脑组织中炎症反应、毛细血管和神经元的结构变化。结果外伤后脑皮层组织含水量呈上升趋势．3h含水量有较大幅度升高，24h达高峰，其后下降，14d时仍处于较高水平，伤后6、12、24、48和72h组与对照组相比．脑组织含水量明显高于对照组（P〈0．05）。脑组织炎症反应、毛细血管和神经元结构变化与脑水肿变化相平行。结论弥漫性颅脑损伤后发生缺血、缺氧．导致微循环障碍，最终血-脑屏障结构破坏，神经细胞的代谢活动紊乱，使脑组织发生继发性脑损伤。弥漫性颅脑损伤后脑水肿是造成继发性脑损伤病理学变化的基础。

Observation of Changes in Brain Edema and Pathology after Diffuse Brain Injury in Rats

Objective To explore the brain edema and histopathological change in brain tissues following diffuse brain injury (DBI) in rats. Methods The model of DBI in rats were established by Marmarou's technique. One hundred male Sprague-Dawley rats were randomly divided into the control group and posttrauma 1 hour, 3 hours, 6 hours, 12 hours, 24 hours, 48 hours, 72 hours, 7 days and 14 days groups of 10 rats each. The water content in the injured brain tissues was determined. The inflammatory reaction and changes in the structures of the capillary and neurons in the injured brain tissues were observed by light and election microscopes. Results The water content of injured brain tissues increased 3 hours after DBI, peaked 24 hours after DBI, and then decreased. The water contents were significantly higher 6, 12, 24, 48 and 72 hours after DBI than in the control group (P<0.05). The inflammatory reaction and changes in the structures of the capillary and neurons were parallel to the change in the water content in the injured brain tissues. Conclusions Ischemic and anoxemia occur after DBI, and then microcirculation disturbance appears. The structure of blood brain barrier is destroyed. At last, the disorder of metabolic activity of neuros produces secondary brain injury. Brain edema after DBI is a basis of the changes in the pathology of secondary brain injury.