Ahmed S A, Williamson J R, Roberts R, Clark R E, Sobel B E
Circulation. 1976 Aug;54(2):187-93. doi: 10.1161/01.cir.54.2.187.
To evaluate the concordance between elevated plasma MB CPK and irreversible myocardial ischemic injury, coronary occlusion was induced for 10 minutes to 48 hours in 21 open chest dogs and 13 conscious animals. Results of plasma CPK and MB CPK assayed in samples obtained serially ofr 24 hours were compared to microscopic changes in hearts from the same animals examined 48 hours after occlusion. Twelve of the 34 dogs died within two hours after coronary occlusion. Among the surviving 22 dogs, one failed to exhibit gross of electrocardiographic evidence of ischemia and was therefore excluded. Twelve had coronary occlusion maintained for 30 minutes or longer and in 11 of these peak plasma MB CPK activity exceeded thenormal range (mean +/- 2 SD) and baseline values by at least 100%. Necrosis was present in the hearts from each manifested by nuclear pyknosis, eosinophilia, shrinkage of cytoplasm, and leukocytic infiltration. In the remaining nine dogs with occlusion for less than 30 minutes, peak plasma MB CPK activity was not elevated and necrosis was not detected. The close concordance between plasma MB CPK elevations and myocardial necrosis was significant (chi2 = 14.5, P less than 0.001), and thus, increased plasma MB CPK activity reflected irreversible myocardial ischemic injury.
为评估血浆肌酸磷酸激酶同工酶（MB CPK）升高与不可逆性心肌缺血损伤之间的一致性，对21只开胸犬和13只清醒动物进行冠状动脉闭塞10分钟至48小时。将连续24小时采集的样本中测定的血浆CPK和MB CPK结果与冠状动脉闭塞48小时后检查的同组动物心脏的微观变化进行比较。34只犬中有12只在冠状动脉闭塞后两小时内死亡。在存活的22只犬中，有1只未表现出缺血的大体或心电图证据，因此被排除。12只犬的冠状动脉闭塞持续30分钟或更长时间，其中11只犬的血浆MB CPK活性峰值超过正常范围（平均值±2标准差）和基线值至少100%。每只犬心脏均出现坏死，表现为核固缩、嗜酸性变、细胞质收缩和白细胞浸润。其余9只冠状动脉闭塞时间少于30分钟的犬，血浆MB CPK活性峰值未升高，也未检测到坏死。血浆MB CPK升高与心肌坏死之间的密切一致性具有显著性（χ2 = 14.5，P < 0.001），因此，血浆MB CPK活性升高反映了不可逆性心肌缺血损伤。
