A study on the mechanism and treatment during lucid interval in a rat model of acute subdural hematoma

使用大鼠急性硬膜下血肿模型（150mul），我们检查了损伤后7天的神经系统后果。大多数大鼠在硬膜下血肿发生后的几个小时内恢复并活动活跃。然而，此后神经功能恶化，约一半的动物在血肿后48小时内死亡。其余大鼠存活7天，恢复基本正常，组织学检查显示血肿下脑梗死。为了区分硬脑膜下血肿的生化效应和肿块效应，在硬脑膜下腔内注射相同体积150mul的惰性硅凝胶，在硬脑膜下注射8小时后灌注固定脑，进行后续的组织病理学检查。硬膜下注射硅胶的大鼠梗死体积明显小于硬膜下血肿的大鼠。关于急性硬膜下血肿的治疗干预，我们检查了脑灌注压的影响和可能有效的药物，包括甲磺酸加贝酸酯、MK-801和氯胺酮。在这些治疗中，只有脑灌注压的影响是显著的。在硬膜下血肿产生过程中，多巴胺输注维持脑灌注压在80 mmHg以上的大鼠，血肿后4天和7天的神经学评分明显优于未输注多巴胺血压支持的大鼠。血肿后8小时脑梗死体积通过MK-801治疗在数值上减少。综上所述，本研究提示脑膜下血肿的弥漫性物质可加重脑损伤，而NMDA拮抗剂可抑制这种损伤，并且在急性脑膜下血肿治疗中维持相对较高的脑灌注压很重要。

Using a rat model of acute subdural hematoma (150mul), we examined neurological consequences for 7 days after the insult. Most of rats recovered and moved actively for a couple of hours after the production of subdural hematoma. However, neurologically deteriorated thereafter and about a half of animals died within 48 hours after hematoma. The remaing rats survived 7 days and recovered nealy normal, although histological examination revealed cerabral infarction under the hematoma in these rats. In order to dintinguish the biochemical effects of thesubdural hematoma from the mass effects, the same volume (150mul) of inert silicone gel was injected into the subdural space and brains were perfused and fixed at 8 hours after the subdural injection for the subsequent histopathological examination. The infarct volume was significantly smaller in rats received subdural injection of silicone compared with rats received subdural hematoma.Conceming therapeutic interventions for acute subdural hematoma, we examined the effects of cerebral perfusion pressure and possibly effective medications including gabexate mesilate, MK-801, and ketamine.Among these treatments, only the effects of cerebral perfusion pressure was significant. In rats whose cerebral perfusion pressure was maintained above 80 mmHg with dopamine infusion during production of subdural hematoma, neurological scores at 4 and 7 days after hematoma were significantly better than those in rats without blood pressure support by dopamine infusion. The volume of cerebral infarct at 8 hours after hematoma was numerically reduced by treatment of MK-801.In conclusion, the present study suggests exacerbation of brain damages due to diffusible substances from the subdural hematoma, which could be inhibited by treatment of NMDA antagonists, and importance of maintenance of relatively high cerebral perfusion pressure during the management of acute subdural hematoma.