CAJ | 학술논문

[目的]探讨凝血酶的直接抑制剂重组双功能水蛭素对大鼠急性心肌梗死后室性心律失常的影响及相关机制.[方法]将70只雄性SD大鼠随机分为10组:水蛭素(HIR)结扎前(HIR 0 min)组,HIR结扎后5 min(HIR 5 min)组,HIR结扎后10 min(HIR 10 min)组,HIR结扎后20 min(HIR 20 min)组,HIR结扎后30 min(HIR 30 min)组),和生理盐水(NS)对应的各时间组,即NS 0 min,NS 5 min,NS 10 min,NS 20 min,NS 30 min,最终每组7只.观察各组室性心律失常的发生情况,Evans法计量各组心梗面积及采用逆转录聚合酶链反应对各组缺血心肌组织的IP3R家族的三种亚型进行测定.[结果] 水蛭素组发生室性心律失常的持续时间及心律失常评分较生理盐水组在结扎后5～20 min均减少(P<0.05);IP3R家族的三种亚型均与心梗后室性心律失常持续时间呈正相关性:但IP3R2 mRNA在结扎后10 min及IP3R3 mRNA在结扎后10 min和20 min,HIR组较NS组下调(P<0.05).[结论]水蛭素有抗心梗后室性心律失常的发生作用,其机制可能为通过IP3R2和IP3R3实现的,而并非IP3R1.
[목적]탐토응혈매적직접억제제중조쌍공능수질소대대서급성심기경사후실성심률실상적영향급상관궤제.[방법]장70지웅성SD대서수궤분위10조:수질소(HIR)결찰전(HIR 0 min)조,HIR결찰후5 min(HIR 5 min)조,HIR결찰후10 min(HIR 10 min)조,HIR결찰후20 min(HIR 20 min)조,HIR결찰후30 min(HIR 30 min)조),화생리염수(NS)대응적각시간조,즉NS 0 min,NS 5 min,NS 10 min,NS 20 min,NS 30 min,최종매조7지.관찰각조실성심률실상적발생정황,Evans법계량각조심경면적급채용역전록취합매련반응대각조결혈심기조직적IP3R가족적삼충아형진행측정.[결과] 수질소조발생실성심률실상적지속시간급심률실상평분교생리염수조재결찰후5～20 min균감소(P<0.05);IP3R가족적삼충아형균여심경후실성심률실상지속시간정정상관성:단IP3R2 mRNA재결찰후10 min급IP3R3 mRNA재결찰후10 min화20 min,HIR조교NS조하조(P<0.05).[결론]수질소유항심경후실성심률실상적발생작용,기궤제가능위통과IP3R2화IP3R3실현적,이병비IP3R1.
[Objective] To determine the effects and possible mechanism of the thrombin antagonist r-RGD-Hirudin (HIR) on ventricular arrhythmia(VA) after acute myocardial infarction (AMI). [Methods] Seventy adult male Sprague-Dawley rats were randomly subjected to the 10 groups according to duration of left coronary occlusion: HIR 0 min, HIR 5 rain, HIR 10 min, HIR 20 min, HIR 30 min, and normal saline(NS) 0 min, NS 5 min, NS 10 min, NS 20 min, NS 30 min; and the average of every group is 7 rats. Acute myocardial infarction was produced by the occlusion of the left anterior descending coronary artery, then the measurements of arrhythmia and infarction sizing by Evans blue were assessed as well as the expression of three isoforms of inositol 1,4,5-trisphosphate receptors (IP3Rs) mRNA in isehemic myocardium by reverse transeriptase polymerase chain reactions (RT-PCR). [Results] Compared with NS groups, the measurements of VA in HIR were reduced significantly in 5 to 20 minutes after AMI (P<0.05). The incidence of VA was all positive related to the expression of three isoforms of IP3Rs mRNA (P<0.01). Compared with NS groups, the expression of type2,inositol 1,4,5-trisphosphate receptor (IP3R2) mRNA at 10 min and type3, inositol 1,4,5-trisphosphate receptor mRNA (IP3R3) at 10 min and 20 min after AMI were significant decreased (P<0.05) in HIR groups. [Conclusion] The thrombin antagonist r-RGD-Hirudin exerts its myocardial protection against ventricular arrhythmia after acute myocardial infarction possible through IP3R2 and IP3R3 and not typel, inositol 1,4,5-trisphosphate receptor (IP3R1).