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

使用急性硬膜下血肿（150 μ l）的大鼠模型，我们检查了损伤后7天的神经学结果。大部分大鼠在硬膜下血肿形成后数小时内恢复活动。然而，此后神经功能恶化，大约一半的动物在血肿后48小时内死亡。其余大鼠均存活7天，基本恢复正常，但组织学检查显示血肿下有脑梗死灶。为了从占位效应中区分硬膜下血肿的生化效应，将相同体积（150 μ l）的惰性硅凝胶注入硬膜下腔，并在硬膜下注射后8小时进行脑灌注和固定，用于随后的组织病理学检查。与接受硬膜下血肿的大鼠相比，接受硬膜下注射硅胶的大鼠的梗死体积显著更小。考虑到急性硬膜下血肿的治疗干预，我们检查了脑灌注压和可能有效的药物（包括甲磺酸加贝酯、MK-801和氯胺酮）的影响。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，多巴胺输注使脑灌注压维持在80 mmHg以上的大鼠，血肿后4天和7天的神经功能评分明显优于未通过多巴胺输注血压支持的大鼠。MK-801治疗后8小时脑梗死体积在数值上减少。总之，本研究表明，急性硬膜下血肿的扩散性物质可加重脑损伤，这可通过NMDA拮抗剂治疗来抑制，并且在急性硬膜下血肿治疗期间维持相对较高的脑灌注压非常重要。

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.