慢性阻塞性肺疾病对心肌损伤及心肌超微结构的影响

摘要

Objective To explore the influence of chronic obstructive pulmonary disease (COPD) on the cardiactroponin-I (cTnI),the antibody of anti-M2 receptor mRNA and myocardial cells ultrastructure .Methods Twenty-four male Wistar rats were divided into three groups randomly:blank group, COPD group, and acute exacerbation of COPD group ( AECOPD group),8 rats in each group.The model of COPD was established by the passive smoking combined with lipopolysaccharide (LPS) dropped into the trachea.Based on the model of COPD,LPS was dropped into the trachea again to establish the acute exacerbation model of COPD .Then ELISA was used to detect the serum level of cTnI ,RT-PCR was used to detect the expression level of the antibody of anti-M2 receptor mRNA ,and the myocardial cells ultrastructure was observed by the electron microscope .Results The serum levels of cTnI and the antibody of anti-M2 receptor mRNA in COPD group were significantly higher than those in the blank group (P<0.05),which were much higher in the AECOPD group in contrast with those in the COPD group and blank group(P<0.05).Compared with blank group,the myocardial ultrastructure showed a mild change in the COPD group under the electron microscope ,and showed a significant change in the AECOPD group . Conclusion COPD might lead to myocardial injury ,and the myocardial ultrastructure might show a mild change .The myocardial injury is more significant in the AECOPD stage .%目的：探讨慢性阻塞性肺疾病（ COPD）对心肌肌钙蛋白I（ cTnI）、抗M2受体抗体mRNA及心肌超微结构的影响。方法健康雄性Wistar大鼠24只，按随机数字表法分为正常组、COPD组、COPD急性加重（ AECOPD）组，每组8只。通过气管内滴入脂多糖和被动吸烟的方法建立COPD模型，COPD模型大鼠再次气管滴入脂多糖建立COPD急性加重模型。酶联免疫吸附测定法法检测血清cTnI水平，反转录-聚合酶链反应检测血中抗M2受体抗体mRNA水平，电子显微镜观察心脏超微结构。结果 COPD组血cTnI、M2受体抗体mRNA水平明显高于正常组（ P＜0．05），而AECOPD组血cTnI、M2受体抗体mRNA水平明显高于COPD组、正常组（ P＜0．05）。与正常组比较，电子显微镜下COPD组心肌超微结构改变轻微， AECOPD组心肌超微结构改变明显。结论 COPD造成心肌损伤，心肌超微结构发生轻微改变，AECOPD期对心肌损伤更加明显。