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目的：研究高粘血症大鼠心肌发生缺血缺氧性损伤时原癌基因c－fos热休克蛋白（Hsp70）表达的变化及意义。方法：用免疫组化法（ABC法）检测高粘血症大鼠心肌组织和体外培养的心肌细胞缺氧后Hsp70和c－fos蛋白变化；用原位杂交法检测c－fosmRNA变化。用光镜、电镜观察心肌组织和心肌细胞的损伤。结果：发现c－fos蛋白在高粘血症大鼠心肌中明显增强，在体外培养的大鼠心肌细胞缺氧1h和4h后较对照组明显增强。c－fosmRNA表达也明显增强。上述变化与细胞损伤间呈正相关。结论：高粘血症引起的缺血缺氧可诱导c－fos表达增强和Hsp70增加，后者可能是心肌对缺血缺氧产生的应激反应产物。它们是一种早期防御代偿反应，并参与调节其他基因的变化。
Objective: To study the changes and significance of c-fos heat shock protein (Hsp70) expression in hypoxic-ischemic myocardium of hyperviscosity rats. Methods: The changes of Hsp70 and c-fos protein in myocardium of hyperviscosity rats and cultured cardiomyocytes were detected by immunohistochemistry (ABC method). The changes of c-fos mRNA were detected by in situ hybridization. Using light microscope and electron microscope to observe the damage of myocardial tissue and cardiomyocytes. Results: The c-fos protein was found to be significantly increased in the myocardium of hyperviscosity rats. Compared with the control group, the cultured rat cardiomyocytes were significantly increased in hypoxia 1h and 4h. c-fos mRNA expression was also significantly enhanced. The above changes were positively correlated with cell injury. Conclusion: Hypoxia induced by hyperviscosity can induce the increase of c-fos expression and increase of Hsp70, which may be the product of stress reaction of myocardial ischemia and hypoxia. They are an early defensive compensatory response and are involved in the regulation of other genetic changes.