Fortier P A, Bedford G K, Chiong M A
Can J Physiol Pharmacol. 1984 Sep;62(9):1158-65. doi: 10.1139/y84-194.
Previous studies have shown that the well-oxygenated perfused rabbit heart releases creatine kinase when treated with the calcium antagonist drug verapamil (VER) in a dose-related manner. It is possible that this effect is related to Ca2+ ion deprivation of the sarcolemma. This possibility was explored by perfusing hearts with low Ca2+ (0.5, 0.23, 0.15, and 0 mM) versus a control group (1.27 mM Ca2+) for 60 min. Low Ca2+ perfusion was associated with reduction in the heart rate--left ventricular systolic pressure product and O2 consumption, tendency for the coronary sinus flow to increase, electromechanical dissociation, prolongation of atrioventricular conduction and QT interval, and decrease in myocardial glycogen. Lower total adenosine nucleotides were found only in the 0 mM Ca2+ group. As the Ca2+ concentration was reduced, the hearts lost increasing amounts of creatine kinase, aspartate aminotransferase, and lactate dehydrogenase. These results confirm the importance of Ca2+ ions in contractile and electrical cardiac functions and show that decreased availability of this cation leads to increasing enzyme leakage resembling that seen in VER-treated hearts.
先前的研究表明，灌注良好且富含氧气的兔心脏在用钙拮抗剂维拉帕米（VER）处理时，会以剂量相关的方式释放肌酸激酶。这种效应可能与肌膜的钙离子剥夺有关。通过用低钙（0.5、0.23、0.15和0 mM）灌注心脏60分钟，并与对照组（1.27 mM钙）进行对比，来探究这种可能性。低钙灌注与心率、左心室收缩压乘积和氧气消耗的降低、冠状窦血流增加的趋势、电机械分离、房室传导和QT间期延长以及心肌糖原减少有关。仅在0 mM钙组中发现总腺苷核苷酸含量降低。随着钙离子浓度的降低，心脏释放出越来越多的肌酸激酶、天冬氨酸转氨酶和乳酸脱氢酶。这些结果证实了钙离子在心脏收缩和电功能中的重要性，并表明这种阳离子可用性的降低会导致酶泄漏增加，类似于在维拉帕米处理的心脏中所见。
