摘要
目的:研究猪急性心肌梗死(AMI)后囊性纤维化跨膜转运调节氯通道(CFTR)和CIC-2型氯通道(CIC-2)基因表达的变化,探讨急性心肌梗死后早期室性心律失常发生的分子机制。方法:通过结扎猪左前降支远端1/3-1/2处2 h然后再灌注建立AMI模型,同时设立相应的假手术(SH)组。术后24 h取左心室梗死边缘区内层(En-do)、中层(Mid)和外层(Epi)心肌(SH组取对应位置心肌),应用逆转录-聚合酶链反应(RT-PCR)半定量分析氯通道CFTR和CIC-2的基因表达的改变。结果:与SH组相比,AMI后梗死边缘区三层心肌CFTR和CIC-2 mRNA表达均明显上升(P<0.05),而且三层心肌间的基因表达呈不均一性(P<0.05)。结论:AMI后梗死边缘区三层心肌氯通道CFTR和CIC-2基因表达的不均一性上调,可能是AMI后早期易发室性心律失常的分子机制之一。
Objective： To investigate the changes of the gene expression of cystic fibrosis transmembrane conductance regulator （CFTR） and CIC-2 chloride channels after acute myocardial infarction （AMI） in pigs. Methods： The pig model of AMI was established by ligating left anterior descending coronary artery for 2 h ischemia before reperfusion. Accordingly, the sham-operation group （sham-group） was established without ligating left anterior descending coronary artery. Using semi-quantitative reverse transcriptase-polymerase chain reaction （RT-PCR）, the mRNA of CFTR and CIC-2 was measured respectively in endocardium （Endo）, midcardium （Mid）and epicardium（Epi） of border zone in each group 24 h later. Results： Compared to the sham-group, CFTR and CIC-2 mRNA in all the three layers of border zone in AMI group remarkably increased respectively（all P〈0.05）, and there were significant differences among three layers（P〈0.05） . Conclusion： The heterogeneous up-regulation of CFTR and CIC-2 chloride channel with mRNA expression may be one of the molecular mechanisms that are able to cause ventricular arrhythmias after acute myocardial infarction.
出处
《武汉大学学报（医学版）》
CAS
2008年第2期149-152,共4页
Medical Journal of Wuhan University
基金
湖北省"十一五"重大科技攻关项目(编号:2006AA301A04)
关键词
心血管病学
心肌梗死
氯通道
室性心律失常
Cardiology
Myocardial Infarction
Chloride Channels
Ventricular Arrhythmia
