大鼠心肌缺血再灌注诱发肺部炎性纤维化

目的探讨大鼠心肌缺血再灌注损伤是否会诱发肺部炎症以及纤维化。方法 Wistar大鼠16只,随机分为假手术组(S组)、心肌缺血再灌注组(IR组),2组均缺血45 min再灌注3 h。实验结束后放血处死大鼠,取肺组织、支气管肺泡灌洗液和血清,测定血清肌酸激酶同工酶(CK-MB)浓度、蛋白含量以及转化生长因子(TGF)-β1浓度,计算肺通透性指数(PPI)、测定肺组织肿瘤坏死因子(TNF)-α蛋白的表达。结果与假手术组比较,心肌缺血再灌注组血清CK-MB活性及TGF-β1浓度均增高,PPI值升高,肺组织TNF-α蛋白表达上调,差异有统计学意义。结论大鼠心肌缺血再灌注可诱发肺部炎性纤维化。

Myocardial ischemia-reperfusion induces lung inflammation and fibrosis in rats

Objective To determine if myocardial infusion-reperfusion （I/R） could induce lung inflammation and fibrosis in rats. Methods Sixteen male Wistar rats were randomly allocated to sham operation （group S） or my- ocardial I/R （group IR） to be subject to ischemia for 45 min and reperfusion for 3 h. All animals were sacrificed by exsanguinations for sampling of the blood, lung tissues and bronchoalveolar lavage （BAL） fluid to determine the levels of MB isoenzyme of creatine kinase （CK-MB）, pulmonary permeability index （PP1）, TNF-α and TGF-β1 expression. Results The levels of serum CK-MB, PPI, TNF-α and TGF-β1 were significantly elevated in group IR compared with the group S （all P〈0.05）. Conclusion Myocardial isehemia-reperfusion injury induces lung inflammation and fibrosis in rats.