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目的：为探讨蛛网膜下腔出血（SAH）后的神经免疫学变化，采用动物实验方法对实验性SAH后不同时间内的TXB2和TNF－α的变化进行了观察。方法：选用Wistar大鼠做SAH实验模型，经颈骨钻孔往入自家血方法完成实验。对不同时间内的血浆TXB2及TNF－α水平做了放免学测定。结果：TXB2在实验后12h即有显著升高（实验前278．0±54．5mmol／L，12～36h间为2714．6±1248．8～3455．5±1496．9），持续至36h后降至正常。TNF－α在实验后12h亦有显著增高，呈持续性（实验前4．6±1．7mmol／L实验后22．8±8．7mmom／L），但在36h和5d有轻度下降，故增高呈双峰型。结论：实验性SAH后TNP有表达增高改变，其机制多与血管内皮损伤和神经组织受损后的合成增加有关，其作用过程与白细胞和血小板的激活过程相关联。TXB2和TNF早期增高的正相关改变提示TNF增高可能在促凝血和血管痉挛中起一定作用。
Objective: To investigate the neuroimmunological changes after subarachnoid hemorrhage (SAH), the changes of TXB2 and TNF-α in different time after experimental SAH were observed by animal experiments. Methods: Wistar rats were selected as experimental model of SAH, and the experiment was completed by drilling into the blood of own blood through the neck bone. The levels of plasma TXB2 and TNF-αin different time were measured by radioimmunoassay. Results: TXB2 was significantly increased at 12h after the experiment (278.0 ± 54.5mmol / L before the experiment and 2714.6 ± 1248.8 ~ 3455.5 ± 1496.9 between 12 ~ 36h), lasting for 36h After falling to normal. TNF-α was also significantly increased 12h after the experiment (before the experiment 4.6 ± 1.7mmol / L after the experiment 22.8 ± 8.7mmom / L), but a slight decrease in 36h and 5d, Therefore, the increase was bimodal. CONCLUSIONS: After experimental SAH, the expression of TNP is increased. The mechanism is mostly related to the increased synthesis of vascular endothelial injury and impaired neural tissue. Its mechanism of action is associated with the activation of leukocytes and platelets. The positive correlation between TXB2 and early TNF suggests that elevated TNF may play a role in procoagulant and vasospasm.