Vaz R, Sarmento A, Borges N, Cruz C, Azevedo T
Institute of Pharmacology and Therapeutics, Mesical Faculty, Hospital S. Joäo, Porto, Portugal.
Acta Neurochir (Wien). 1998;140(1):76-81. doi: 10.1007/s007010050061.
Several experimental brain oedema models are currently available, but most of them are very different from what happens in clinical practice. As it is simple and seems to replicate the range of injuries seen in man we decided to evaluate Marmarou's model of head injury in order to test physiopathogenic and therapeutic hypotheses. Three groups of Wistar rats weighting 360-400 gr, anaesthetized with sodium pentobarbitone and breathing spontaneously, without tracheal intubation, were studied. In the first group six animals were killed two hours after injury and the brain's water content compared with that of nine controls. In another group Evans blue (100 mg/kg) was injected one hour before trauma and dye's extraction ratio determined at various times after injury: five animals at 15 minutes, six at 30 minutes, five at 60 minutes and nine at 120 minutes. A total of twenty-eight animals served as controls. In the last group morphological studies with light and electron microscopy were performed in the traumatized brain tissue from rats killed 5 and 120 minutes after injury and in brain tissue from control rats. Results showed that Marmarou's brain trauma model induced perivascular brain oedema, already visible at the ultrastructural level 5 minutes after the injury. Endothelial cells themselves were "oedematiated", rich in pinocytotic vesicles and membrane blebs, and presented intact tight junctions. Two hours after trauma the perivascular oedema was more marked. At this time the brain water content was significantly higher than that in controls. Evans blue extraction ratio increased linearly with time, being significantly higher than in controls 120 minutes after injury. We conclude that Marmarou's model is a suitable model for the study of brain oedema induced by trauma, and that this oedema, assessed by three different methodologies, was statistically significant two hours after injury.
目前有几种实验性脑水肿模型，但其中大多数与临床实践中的情况有很大不同。由于其操作简单且似乎能复制人类所见的损伤范围，我们决定评估马尔马罗的头部损伤模型，以检验生理病理和治疗假设。研究了三组体重360 - 400克的Wistar大鼠，用戊巴比妥钠麻醉，自主呼吸，未行气管插管。第一组中，六只动物在受伤两小时后处死，将其脑含水量与九只对照动物的进行比较。在另一组中，在创伤前一小时注射伊文思蓝（100毫克/千克），并在受伤后的不同时间测定染料提取率：15分钟时五只动物，30分钟时六只，60分钟时五只，120分钟时九只。共有二十八只动物作为对照。在最后一组中，对受伤后5分钟和120分钟处死的大鼠的创伤脑组织以及对照大鼠的脑组织进行了光镜和电镜形态学研究。结果显示，马尔马罗的脑创伤模型诱发了血管周围脑水肿，在损伤后5分钟的超微结构水平就已可见。内皮细胞本身出现“水肿”，富含吞饮小泡和膜泡，紧密连接完整。创伤两小时后，血管周围水肿更明显。此时脑含水量显著高于对照组。伊文思蓝提取率随时间呈线性增加，在受伤120分钟后显著高于对照组。我们得出结论，马尔马罗模型是研究创伤性脑水肿的合适模型，并且通过三种不同方法评估的这种水肿在受伤两小时后具有统计学意义。
