Yasmineh W G, Pyle R B, Cohn J N, Nicoloff D M, Hanson N Q, Steele B W
Circulation. 1977 May;55(5):733-7. doi: 10.1161/01.cir.55.5.733.
Serum CPK-MB iosenzyme activity was measured serially after mercury embolization of the left circumflex coronary artery in five baboons and after clinical acute myocardial infarction (AMI) in 20 patients. The calculated amount of enzyme released into the baboons' circulation (CPK-MBR) correlated well (r = 0.991) with the amount of MB isoenzyme depleted from the myocardium (CPK-MBD) when a previously determined decay constant (Kd) was used, but not when Kd was calculated from individual curves or when CPK-MM values were used. In clinical AMI, CPK-MMR averaged 97% (0 to 350%) greater than CPK-MBR, probably because of release of MM isoenzyme from nonmyocardial sources. The mean Kd for CPK-MB in patients (0.0012 min-1) was significantly (P less than 0.01) lower than that obtained in the baboon following bolus injections (0.0018 min-1), probably reflecting delayed myocardial release of enzyme. Therefore, in both experimental and clinical AMI, serial samples for CPK-MB activity, but not total or CPK-MM activity, could provide an accurate index of myocardial enzyme depletion.
在5只狒狒的左旋冠状动脉汞栓塞后以及20例临床急性心肌梗死(AMI)患者发病后,连续测量血清肌酸磷酸激酶同工酶(CPK-MB)活性。当使用先前确定的衰变常数(Kd)时,计算得出的释放到狒狒循环中的酶量(CPK-MBR)与心肌中消耗的MB同工酶量(CPK-MBD)相关性良好(r = 0.991),但当根据个体曲线计算Kd或使用CPK-MM值时则不然。在临床AMI中,CPK-MMR平均比CPK-MBR高97%(0至350%),这可能是由于MM同工酶从非心肌来源释放所致。患者中CPK-MB的平均Kd(0.0012分钟-1)显著低于(P < 0.01)推注后狒狒的Kd(0.0018分钟-1),这可能反映了心肌酶释放延迟。因此,在实验性和临床AMI中,连续采集CPK-MB活性样本(而非总活性或CPK-MM活性样本)可提供心肌酶消耗的准确指标。