辛伐他汀对大鼠心肌梗死后交感神经重构和室性心律失常的影响

Effects of simvastatin on sympathetic remodeling and ventricular arrhythmias in rats with myocardial infarction

目的:探讨辛伐他汀对大鼠心肌梗死后交感神经重构和室性心律失常的影响。方法:将SD大鼠48只随机分为假手术组(A组)、心梗组(B组)、辛伐他汀组(C组)。行电生理检查,免疫组化法检测梗死边缘区酪氨酸羟化酶和生长相关蛋白-43阳性神经纤维密度和分布。RT-PCR法检测神经生长因子和白细胞介素-1β以及肿瘤坏死因子-α基因表达。结果:与A组比较,阳性神经纤维密度在B组明显增加(均P<0.05),目标基因表达亦增加(均P<0.05);室性心律失常诱发率明显升高(P<0.05)。C组阳性神经纤维密度和基因表达以及室性心律失常诱发率均较B组减少(均P<0.05)。结论:辛伐他汀通过减少心肌梗死大鼠交感神经重构而起到预防室性心律失常的作用,其机制可能与减少炎症和NGF表达下调有关。

Objective To investigate the effects of simvastatin on cardiac sympathetic remodeling and ventricular arrhythmias （VA） in rats with myocardial infarction （MI）. Methods 48 SD rats were randomized to 3 groups： sham operation group （Group A）, MI group （Group B）, and simvastatin group （Group C）. Immunohistochemistry was used to detect the distribution and density of growth associated protein-43 and tyrosine hydroxylase positive nerve in infarction border zone. Expressions of nerve growth factor, interleukin-1β, and tumor necrosis factor-α were detected by RT-PCR. Results As compared with those in Group A and C, the densities of positive nerve, targeted factors, and the incidence of VA were significantly higher in Group B （P 〈 0.05）. Conclusion Simvastatin can prevent VA through improving sympathetic remodeling in rats with MI, the mechanism may be related to reducing inflammation and the expression of NGF.