CAJ | 학술논문

目的应用应变/应变率成像(S/SRI)及基质金属蛋白酶-9(MMP-9)蛋白表达评价心肌梗死后心力衰竭(心衰)大鼠心肌收缩功能及心室重构.方法 70只雄性SD大鼠随机分为4组:手术4周组及手术8周组,开胸结扎左冠状动脉前降支;假手术组,同样开胸,但不结扎;正常组作为对照.应用S/SRI定量评价心肌局部收缩功能,用Western blot法检测各组实验大鼠心肌MMP-9蛋白表达.结果 (1)除下壁中间段及基底段外,手术4周组各节段收缩期峰值应变、收缩期峰值应变率、收缩末期应变均明显下降(P<0.05),收缩后应变指数升高(P<0.05);手术8周组各指标值较手术4周组变化更明显(P<0.05).(2)手术4周组和手术8周组大鼠心肌MMP-9蛋白的表达明显增加(P<0.05),且手术8周组MMP-9蛋白的表达高于手术4周组(P<0.05).结论 S/SRI技术可定量检测心衰大鼠局部心肌收缩功能,在术后8周内大鼠心肌组织MMP-9蛋白的表达随心衰的进展而增高.
목적 응용응변/응변솔성상(S/SRI)급기질금속단백매-9(MMP-9)단백표체평개심기경사후심력쇠갈(심쇠)대서심기수축공능급심실중구.방법 70지웅성SD대서수궤분위4조:수술4주조급수술8주조,개흉결찰좌관상동맥전강지;가수술조,동양개흉,단불결찰;정상조작위대조.응용S/SRI정량평개심기국부수축공능,용Western blot법검측각조실험대서심기MMP-9단백표체.결과 (1)제하벽중간단급기저단외,수술4주조각절단수축기봉치응변、수축기봉치응변솔、수축말기응변균명현하강(P<0.05),수축후응변지수승고(P<0.05);수술8주조각지표치교수술4주조변화경명현(P<0.05).(2)수술4주조화수술8주조대서심기MMP-9단백적표체명현증가(P<0.05),차수술8주조MMP-9단백적표체고우수술4주조(P<0.05).결론 S/SRI기술가정량검측심쇠대서국부심기수축공능,재술후8주내대서심기조직MMP-9단백적표체수심쇠적진전이증고.
Objective To evaluate the myocardial systolic function and ventricular remodeling in heart failure rat induced by myocardial infarction (MI) with S/SRI and MMP-9. Methods A total of 70 male SD rats were randomly assigned to 4 groups: 4 weeks and 8 weeks MI ( anterior descending branch of left coronary artery were ligated ) , sham operation (thoracotomy without ligation of coronary artery ) and nonoperated control group. The regional myocardial systolic function of rats was quantified with S/SRI. The myocardial MMP-9 expression was detected by Western blot Results In the 4 weeks MI group, all segment's Ssys, SRsys, the strain of end-systole were reduced while PSI was increased compared to sham and nomoperated group with the exception of the inferior wall. These changes were more significant in 8 weeks MI group compared to the 4 weeks MI group. In the 4 weeks MI group, the expression of MMP-9 was significantly upregulated than the sham operation group and this upregulation was more significant at 8 weeks post MI. Conclusions S/SRI can quantitative evaluate the regional systolic function of heart failure rat induced by myocardial infarction. Progressive upregulation of myocardial MMP-9 expression paralleled the deterioration of regional systolic function in this heart failure rat model.