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目的探讨心肌缺血再灌注损伤导致心室重构的发生机制。方法建立家兔心肌缺血再灌注模型,采用免疫组化,HE染色,血流动力学检测等技术,观察p53、bcl-2c、-myc基因蛋白表达在心肌重构中的作用。结果(1)p53、bcl-2基因蛋白共同调控心肌细胞凋亡,在IR后4 h达到高峰,与对照组比较有极显著的差异(P<0.01)。影响了血流动力学改变。(2)c-myc基因蛋白在缺血再灌注后4~8 h达到高峰。与对照组比较有极显著的差异(P<0.01)。导致心肌细胞肥大。结论在心肌缺血再灌注过程中p53、bcl-2、c-myc基因蛋白的表达导致了心室的重构。
Objective To investigate the mechanism of ventricular remodeling induced by myocardial ischemia-reperfusion injury. Methods Myocardial ischemia-reperfusion model in rabbits was established. The expression of p53, bcl-2c and -myc in myocardial remodeling was observed by immunohistochemistry, HE staining and hemodynamics. Results (1) The p53 and bcl-2 gene proteins could regulate the apoptosis of cardiomyocytes, which peaked at 4 h after IR. There was a significant difference compared with the control group (P <0.01). Affect hemodynamic changes. (2) c-myc protein peaked 4 ~ 8 h after ischemia-reperfusion. Compared with the control group, there was a significant difference (P <0.01). Causes cardiomyocyte hypertrophy. Conclusion The expression of p53, bcl-2 and c-myc gene proteins during myocardial ischemia / reperfusion leads to ventricular remodeling.