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目的：探讨热休克反应对大鼠缺血-再灌心肌保护作用的可能机制。方法：SD大鼠，随机分为对照组及热休克组，动物经热休克处理恢复2或24h后复制缺血再灌模型并进行各项检测。结果：①热休克处理后心肌组织内SOD活性显著高于对照组，MDA含量则显著低于对照组。②热休克组心肌组织内乳酸及ATP含量均显著高于对照组，糖原含量则显著低于对照组。③热休克反应能诱导HSP70i的转录。结论：热休克反应对缺血-再灌心肌的保护作用与心肌能量代谢的改善、抗氧化能力的增强以及HSP70i的转录合成增强有关。
Objective: To investigate the possible mechanism of heat shock response to myocardial ischemia-reperfusion injury in rats. Methods: SD rats were randomly divided into control group and heat shock group. Animals were subjected to heat shock treatment for 2 or 24 hours after ischemia-reperfusion. Results: ① The activity of SOD in myocardium after heat shock treatment was significantly higher than that in control group, and the MDA content was significantly lower than that in control group. ② The contents of lactic acid and ATP in heat shock group were significantly higher than those in control group, and glycogen content was significantly lower than that in control group. ③ heat shock response can induce HSP70i transcription. CONCLUSION: The protective effect of heat shock on myocardial ischemia-reperfusion injury is related to improvement of myocardial energy metabolism, enhancement of antioxidant capacity and enhancement of transcriptional synthesis of HSP70i.