阿托伐他汀对冠状动脉微栓塞后非梗死区心肌炎症的影响

Roles of atorvastatin in myocardial inflammation of uninfarcted area following coronary microembolization

目的:探讨阿托伐他汀干预治疗对冠状动脉微栓塞(CME)后非梗死区心肌炎症的影响。方法:给清洁级雄性新西兰兔选择性经左前降支(LAD)注入微栓子颗粒悬液建立CME模型,将36只新西兰兔随机分为CME组(模型组)、阿托伐他汀(atrovastatin)干预组及对照组,每组12只(n=12)。于术后7 d处死,取左心室乳头段心肌经HE染色后,观察梗死心肌并检测梗死面积。用ELISA法及RT-PCR检测肿瘤坏死因子α(TNF-α)、白介素6(IL-6)及其基因在非梗死区(右室)心肌中的表达。结果:前降支动脉微栓塞后,非梗死区右室心肌中白细胞浸润明显增多,TNF-α、IL-6蛋白及其基因的表达显著增强。与未处理组相比,阿托伐他汀可显著抑制CME后右室心肌中白细胞浸润及TNF-α、IL-6蛋白及其基因的表达(均P<0.01)。结论:冠脉微栓塞后,炎症反应的激活不仅局限于梗死灶,且累及非梗死区心肌。阿托伐他汀可显著抑制CME后非梗死区心肌炎症反应。

AIM： To investigate the roles of atorvastatin in myocardial inflammation of uninfarcted area following coronary microembolization （CME）. METHODS： CME model in rabbits was established by injecting homologous microthrombotic particle suspension into the left descending anterior branch （LAD）. Thirty-six New Zealand rabbits were randomized to untreated CME group, atorvastatin-treated CME group and sham operation group （n = 12/group）. Rabbits were sacrificed on postoperative day 7. The morphological characteristics were evaluated in sections with H/E staining and protein and gene expressions of TNFα and IL-6 were semiquantitatively analyzed by ELISA and RT-PCR. RESULTS： LAD mieroembolization produced increased leukocyte infiltration and strong TNFα, IL-6 mRNA and protein expressions in uninfarcted right ventricular myocardium. Atorvastatin significantly suppressed the inflammatory cell infiltration and protein and gene expression of TNFα and IL-6 （P 〈0.01 ）. CONCLUSION： Coronary microembolization produces myocardial inflammatory activation, which is not only confined to the microinfarcted zones but also the uninfarcted area. Atorvastatin markedly suppresses TNFα, IL-6 protein and gene expressions and effectively ameliorates myocardial inflammation in the uninfarcted area.