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目的探讨热应激反应对大鼠感染性脑水肿的保护机制。方法将大鼠进行热休克预处理后，采用百日咳菌液所致的感染性脑水肿模型，观察脑匀浆上清液中肿瘤坏死因子α（ＴＮＦα）、一氧化氮（ＮＯ）水平的变化。结果感染性脑水肿的脑组织含水量、脑匀浆ＴＮＦα含量及ＮＯ浓度均增高，热休克预处理可降低脑组织含水量、ＴＮＦα含量及ＮＯ浓度；脑组织含水量与ＴＮＦα含量及ＮＯ浓度呈正相关，相关系数分别为０．４５８和０．７６２。结论热应激反应能减轻感染性脑水肿的发生，其机理可能与ＨＳＰ７０表达增加，抑制ＮＯ及ＴＮＦα生成有关
Objective To investigate the protective mechanism of heat stress on infectious brain edema in rats. Methods After heat shock preconditioning in rats, the model of infectious brain edema caused by pertussis bacilli was used to observe the changes of tumor necrosis factor α (TNFα) and nitric oxide (NO) in brain homogenate supernatant. Results Brain water content, brain TNF-α content and NO concentration in infectious brain edema were increased. Heat shock preconditioning could decrease brain water content, TNFα content and NO concentration. Brain water content and TNFα content and NO concentration were positive The correlation coefficients were 0.458 and 0.762, respectively. Conclusion Heat stress can reduce the occurrence of infectious brain edema. The mechanism may be related to the increase of HSP70 expression and the inhibition of the production of NO and TNFα