CAJ | 학술논문

目的研究大鼠心肌经历缺血再灌注损伤后心功能指标的变化，探讨缺血后处理是否具有保护作用，并探寻STAT3在其中的作用机制。方法 SD大鼠32只，随机分为4组：对照组、缺血再灌注组、缺血后处理组、缺血后处理组+NSC-74859( STAT3抑制剂)组。建立大鼠离体心脏工作模型，观察心脏在各组条件下心率、LVSP、+dp/dtmax、-dp/dtmax、冠脉流量的变化及心肌酶谱的改变。结果缺血后处理组与缺血再灌注组相比，复灌期心率，冠脉流出液中CK 及LDH 的含量明显降低，左室收缩压、左心室压力变化率、冠状动脉流出量明显升高。而抑制STAT3表达后，此保护效应明显减弱。结论缺血后处理有助于减轻缺血再灌注所致心肌损伤，这一作用由STAT3转录因子介导。
목적연구대서심기경력결혈재관주손상후심공능지표적변화，탐토결혈후처리시부구유보호작용，병탐심STAT3재기중적작용궤제。방법 SD대서32지，수궤분위4조：대조조、결혈재관주조、결혈후처리조、결혈후처리조+NSC-74859( STAT3억제제)조。건립대서리체심장공작모형，관찰심장재각조조건하심솔、LVSP、+dp/dtmax、-dp/dtmax、관맥류량적변화급심기매보적개변。결과결혈후처리조여결혈재관주조상비，복관기심솔，관맥류출액중CK 급LDH 적함량명현강저，좌실수축압、좌심실압력변화솔、관상동맥류출량명현승고。이억제STAT3표체후，차보호효응명현감약。결론결혈후처리유조우감경결혈재관주소치심기손상，저일작용유STAT3전록인자개도。
Objective To research ischemic postconditioning on heart function after myocardial ischemia-reperfusion(I/R),and the protective mechanisms. Methods Thirty-two rats were divided into four groups:I/R group ( n = 8 ) , ischemic postconditioning group (n=8),myocardial ischemic postconditioning+ NSC-74859 (STAT3 inhibitor) group(n=8),and control group(n=8). Establish a model of rat to observe changes of the heart rate,LVSP,+dp/dtmax,-dp/dtmax,coronary flow and myocardial enzyme spectrum in each group un-der different conditions. Results Compared with ischemia-reperfusion group,heart rate of the reperfusion period,CK and LDH of coronary ef-fluent in the ischemic postconditioning group were obviously lower,while left ventricular systolic pressure,change of intraventricular pressure, and coronary effluent volume increased obviously. And after inhibition of STAT3 expression,this protective effect decreased significantly. Con-clusion Ischemic postconditioning can provide potent cardioprotective effect in which STAT3 mediates the cardioprotective effects.