CAJ | 학술논문

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。
목적：탐토만성조새성폐질병（ COPD）대심기기개단백I（ cTnI）、항M2수체항체mRNA급심기초미결구적영향。방법건강웅성Wistar대서24지，안수궤수자표법분위정상조、COPD조、COPD급성가중（ AECOPD）조，매조8지。통과기관내적입지다당화피동흡연적방법건립COPD모형，COPD모형대서재차기관적입지다당건립COPD급성가중모형。매련면역흡부측정법법검측혈청cTnI수평，반전록-취합매련반응검측혈중항M2수체항체mRNA수평，전자현미경관찰심장초미결구。결과 COPD조혈cTnI、M2수체항체mRNA수평명현고우정상조（ P＜0．05），이AECOPD조혈cTnI、M2수체항체mRNA수평명현고우COPD조、정상조（ P＜0．05）。여정상조비교，전자현미경하COPD조심기초미결구개변경미， AECOPD조심기초미결구개변명현。결론 COPD조성심기손상，심기초미결구발생경미개변，AECOPD기대심기손상경가명현。
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 .