The control of myocardial Ca++ sequestration with nifedipine cardioplegia

Abstract

Myocardial 45Ca sequestration was studied in dogs after an injection of 45CaCl2 during 60 minutes of global ischemia and 30 minutes of reperfusion using cardiopulmonary bypass (CPB) at 32 degrees C. Group I (n = 10) received a standard hyperkalemic cardioplegic solution and Group II (n = 10) received the same cardioplegia solution plus nifedipine (100 micrograms/300 cc). After aortic cross-clamping, 300 cc of cardioplegic solution was delivered at 0 and 30 minutes at 4 degrees C. Tissue specific activity (SA = cpm x 10(4)/gm) and plasma specific activity (SA = cpm x 10(4)/ml) were determined before release of the cross-clamp and serially by biopsy during reperfusion. The ratio of tissue SA to plasma SA, termed relative specific activity (RSA), indicates myocardial 45Ca sequestration. Nifedipine led to a marked decrease in sequestration. Group II RSAs were 31.5%, 82.1%, and 39.6% less than Group I RSAs at 0, 20, and 30 minutes of reperfusion. All differences were highly significant (p less than 0.01). During the first 20 minutes of reperfusion, the Group I RSA increased 498% while the Group II RSA increased only 23.8%. A correlation is shown between the decreased calcium sequestration and improved myocardial performance after CPB, demonstrated in previous experiments using nifedipine. Nifedipine in combination with a hypothermic hyperkalemic cardioplegic solution effectively controls myocardial calcium sequestration during 60 minutes of ischemia arrest and the immediate 30 minutes of reperfusion.