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目的建立海水浸泡颅脑挫裂伤模型,观察海水浸泡对实验性脑挫裂伤后创伤性脑水肿的影响及研究兔脑挫伤后不同时间caspase-8及caspase-3表达的变化。方法采用立体定向自由落体伤模型进行持续海水浸泡作为实验组,对照组采用同样的方法致伤后不进行海水浸泡。观察创伤组织的病理改变,并通过免疫组化染色和计算机图像分析技术用半定量化的方法检测不同干预不同时程caspase-8和caspase-3的活性表达强弱差异。结果实验组和对照组均发生了创伤性脑水肿,但水肿高峰期出现时间不一致,严重程度也不一致。实验组caspase-8和caspase-3活性表达强度均高于对照组。结论海水浸泡促进了挫裂伤周边缺血水肿区神经细胞凋亡的增加。
Objective To establish a model of craniocerebral contusion and laceration in seawater so as to observe the effect of seawater immersion on traumatic brain edema after experimental cerebral contusion and laceration and to study the changes of caspase-8 and caspase-3 expression at different time points following brain contusion in rabbits. Methods Stereotactic free-fall injury model was used to treat continuous seawater immersion as the experimental group, while the control group was treated with the same method without seawater immersion. The pathological changes of wound tissues were observed. The differences of the expression of caspase-8 and caspase-3 in different time courses were detected by semi-quantitative method by immunohistochemistry and computer image analysis. Results Traumatic brain edema occurred in both experimental group and control group, but the echogenic time was inconsistent and the severity was inconsistent. The experimental group of caspase-8 and caspase-3 activity were higher than the control group. Conclusion Seawater immersion promotes the increase of nerve cell apoptosis in the ischemic and edema area around contusion and laceration.