Isobe M, Nagai R, Yamaoki K, Nakaoka H, Takaku F, Yazaki Y
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Circ Res. 1989 Sep;65(3):684-94. doi: 10.1161/01.res.65.3.684.
The effects of early coronary artery reperfusion on the relation between the extent of myocardial infarction and serum levels of cardiac myosin light chain II or plasma creatine kinase levels were evaluated in the conscious dog. Hydraulic occluders were placed on the left anterior descending arteries of 38 dogs. Seven to 10 days later, myocardial infarction was produced. Coronary reperfusion was performed 3 hours (group A1, n = 13) and 6 hours (group A2, n = 12) after the occlusion. In the other 13 dogs, coronary occlusion was sustained throughout the course of the experiment (group B). Seven days after the occlusion, the heart was cut from the apex to the base into 4-mm slices, and infarct size was determined macroscopically. Rapid appearance and early peaking of creatine kinase were observed in group A. Cumulative release of creatine kinase significantly correlated with infarct size in group A (infarct size ranged from 0.1 to 20.1 g, r = 0.90) and group B (from 0.6 to 26.8 g, r = 0.91). However, since creatine kinase release in group A was greater in comparison with that from infarcts of the same size in group B, the slope of the regression line for group A was significantly steeper (p less than 0.05). Cardiac myosin light chain II appeared as early as creatine kinase did and continued to be elevated for 7 days. A very close relation was observed between infarct size and total cardiac myosin light chain II release (r = 0.87 for group A, and r = 0.88 for group B) or peak level of light chain II (r = 0.85 for group A, and r = 0.81 for group B). In addition, the slopes of the regression lines for infarct size and both peak and total release of light chain II did not differ between group A and group B. On histological examination, viable myocardium was frequently observed in the epicardium of the ischemic area in group A1; therefore, infarct size was greater in group B than in group A1 (p less than 0.05). Also, myocardial creatine kinase content in the epicardium of the center of the ischemic area in group A1 was greater than that in group B. Cardiac myosin light chain II release in group A1 was less than that in group B, whereas no difference was found in plasma creatine kinase release among groups A1, A2, and B.(ABSTRACT TRUNCATED AT 250 WORDS)
在清醒犬中评估早期冠状动脉再灌注对心肌梗死范围与血清心肌肌球蛋白轻链II水平或血浆肌酸激酶水平之间关系的影响。将液压阻塞器置于38只犬的左前降支动脉上。7至10天后，造成心肌梗死。在阻塞后3小时（A1组，n = 13）和6小时（A2组，n = 12）进行冠状动脉再灌注。另外13只犬在整个实验过程中持续冠状动脉阻塞（B组）。阻塞7天后，将心脏从心尖到基部切成4毫米厚的切片，宏观测定梗死面积。A组观察到肌酸激酶快速出现并早期达到峰值。A组（梗死面积范围为0.1至20.1克，r = 0.90）和B组（0.6至26.8克，r = 0.91）中肌酸激酶的累积释放与梗死面积显著相关。然而，由于A组中肌酸激酶的释放比B组中相同大小梗死的释放更大，A组回归线的斜率明显更陡（p小于0.05）。心肌肌球蛋白轻链II与肌酸激酶一样早出现，并持续升高7天。观察到梗死面积与心肌肌球蛋白轻链II总释放量（A组r = 0.87，B组r = 0.88）或轻链II峰值水平（A组r = 0.85，B组r = 0.81）之间存在非常密切的关系。此外，A组和B组之间梗死面积与轻链II峰值及总释放量的回归线斜率没有差异。组织学检查显示，A1组缺血区心外膜中经常观察到存活心肌；因此，B组梗死面积大于A1组（p小于0.05）。而且，A1组缺血区中心心外膜中的心肌肌酸激酶含量高于B组。A1组中心肌肌球蛋白轻链II的释放低于B组，而A1组、A2组和B组之间血浆肌酸激酶释放没有差异。（摘要截断于250字）
