Depressed Myocardial Creatine Phosphokinase Activity Following Experimental Myocardial Infarction in Rabbit
Depressed Myocardial Creatine Phosphokinase Activity Following Experimental Myocardial Infarction in Rabbit
复制标题
兔实验性心肌梗死后心肌肌酸磷酸激酶活性降低
作者：
J. Kjekshus;B. Sobel
由于肌酸磷酸激酶（CPK）主要存在于心肌和骨骼肌细胞中，与参与炎症反应的细胞相反，因此认为测量心脏中该酶的活性可能会提供急性冠状动脉闭塞后缺血性损伤程度的敏感且相对特异的指标。因此，连续测定冠状动脉闭塞后，从兔心肌梗死和正常兔左心室提取物中的CPK活性。此外，在结扎冠状动脉后24小时，测定了犬心脏各部分提取物中的心肌CPK活性。家兔心肌梗塞后6小时内CPK活性均明显降低。24小时后，活性从15.5±0.9（平均值±SE）降至3.4±0.3。在整个左心室提取物中CPK活性被抑制，一般来说，抑制的程度与总梗死面积成正比。冠状动脉闭塞后24小时犬心脏各区域CPK抑制与使用放射性标记微球测定的血流减少程度相关。结果表明，抑郁症的心肌CPK活性可能是有用的，在估计组织损伤的程度，实验性冠状动脉闭塞和预防和治疗措施对心肌的生存在这种情况下的效果。
Since creatine phosphokinase (CPK) is found predominantly in myocardial and skeletal muscle cells, in contrast to cells participating in the inflammatory response, it was considered likely that measurement of activity of this enzyme in the heart would provide a sensitive and relatively specific index of the extent of ischemic injury following acute coronary artery occlusion. Accordingly, CPK activity was measured serially following coronary artery occlusion in extracts from rabbit myocardium with gross infarction and from normal rabbit left ventricle. In addition, myocardial CPK activity was assayed in extracts from various portions of dog hearts 24 hours after ligation of the coronary artery. CPK activity of rabbit myocardium with infarction was uniformly depressed within 6 hours following coronary occlusion. After 24 hours, activity declined from 15.5±0.9 (mean±SE) to 3.4±0.3. CPK activity in whole left ventricular extracts was depressed and in general, the extent of depression was proportional to the size of the gross infarct. CPK depression in various regions of the dog heart 24 hours after coronary occlusion correlated with the extent of reduction of blood flow determined with the use of radioactively labeled microspheres. Results suggest that depression of myocardial CPK activity may be useful in estimating the extent of tissue damage following experimental coronary artery occlusion and the effect of prophylactic and therapeutic measures on the survival of myocardium in this setting.