大鼠急性心肌缺血诱发肺损伤的信号机制

Signaling of lung injury induced by myocardial ischemia-reperfusion in rats

目的探寻大鼠急性心肌缺血再灌注后诱发肺损伤的信号机制。方法 12只健康雄性Wistar大鼠随机分为2组(n=6):心肌缺血再灌注组(C组)和假手术组(S组)。采用活结结扎冠状动脉左前降支(LAD)的方法制备心肌缺血再灌注模型。C组阻断LAD45min后再灌注3h;S组缝合针仅穿过LAD下方,不结扎。分别于实验结束时放血处死大鼠,提取肺组织、支气管肺泡灌洗(BAL)液和血清;进而测定血清肌酸激酶同工酶(CK-MB)、计算肺通透性指数(PPI)、蛋白印迹法检测肺组织转化生长因子(TGF)-β1和肿瘤坏死因子(TNF)-α蛋白的含量。结果与S组相比,C组CK-MB和PPI明显升高;同时TGF-β1和TNF-α蛋白含量增加。结论大鼠心肌缺血再灌注后肺组织TGF-β1和TNF-α蛋白含量明显增加。

Objective To investigate the signaling of lung injury induced by myocardial ischemia-reperfusion （I/R） in rats. Methods Twelve male Wistar rats were randomly allocated to myocardial I/R group （group C） and Sham operation group （group S）, respectively. Myocardial I/R models were prepared via ligation of left anterior descending coronary artery （LAD） by using a running loop. LAD was occluded for 45 minutes followed by a 3-hour reperfusion in group C, while in group S the suture needle was threaded through LAD without ligation. All animals were sacrificed by exsanguination at the end of operation. The lung tissues, bronchoalveolar lavage （BAL） fluid and serum were collected for determination of serum creatinine kinase isoenzyme （CK-MB） and pulmonary permeability in- dex （PPI）. The level of TGF-β1 and TNF-α in pulmonary tissues was assessed by Western blotting. Results Group C was featured of markedly increased （all P〈0.05） levels of serum CK-MB, PPI, TGF-β1 and TNF-α as compared with group S. Conclusion Myocardial I/R is associated with considerably increased TGF-β1 and TNF-α levels in pul- monary tissues in rats.