目的:脑梗死和脑出血是脑血管病的主要疾病,发病后造成的缺血性脑损伤机制迄今尚未完全阐明。肿瘤坏死因子(TNF-α)是重要免疫调节功能的细胞因子,是机体炎症和免疫应答的重要介质,目前已成为基础和临床的研究热点,越来越多的证据表明TNF-α参与脑缺血损伤机制。本文从临床角度探讨了TNF-α在脑血管不病同时期的作用机制。方法:利用ELISA双抗体夹心法分别测定脑梗死及脑出血患者急性期、稳定期和恢复期中TNF-α的含量变化。结果:脑梗死和脑出血患者血浆中TNF-α含量在急性期和稳定期均明显高于恢复期和正常对照组水平。脑梗死和脑出血中TNF-α含量变化同期无显著差异。随出血量增大,TNF-α含量有增高趋势,大灶与小灶比较有显著差异,大、小灶与中灶比较无显著差异。结论:TNF-α在脑梗死和脑出血后均升高,说明它参与了机体的病生理变化过程,在脑缺血损害中有保护和破坏的双重作用。 Objective: Cerebral infarction and cerebral hemorrhage are the main diseases of cerebrovascular disease. The pathogenesis of ischemic brain injury after the onset has not yet been fully elucidated. Tumor necrosis factor (TNF-α) is an important immune regulatory cytokine and an important mediator of inflammation and immune response in the body. At present, TNF-α has become a hot spot in basic and clinical research. More and more evidences indicate that TNF-α participates in brain deficits Blood damage mechanism. This article from the clinical point of view of TNF-α in cerebrovascular disease at the same period the mechanism of action. Methods: The levels of TNF-α in acute phase, stable phase and convalescent phase of cerebral infarction and cerebral hemorrhage were detected by ELISA double antibody sandwich method respectively. Results: The levels of plasma TNF-αin patients with cerebral infarction and intracerebral hemorrhage were significantly higher than those in convalescent and normal controls in both acute phase and stable phase. There was no significant difference in TNF-α content between cerebral infarction and intracerebral hemorrhage during the same period. With the increase of blood loss, the content of TNF-αincreased, the difference between large and small lesions was significant, and there was no significant difference between large and small lesions and middle lesions. CONCLUSION: TNF-α is increased after cerebral infarction and intracerebral hemorrhage, indicating that it is involved in the pathophysiology of the disease and has the dual role of protection and destruction in cerebral ischemia.