NORMOTHERMIC VERSUS HYPOTHERMIC HYPERKALEMIC CARDIOPLEGIA - EFFECTS ON MYOCYTE CONTRACTILITY

Background. This study was designed to determine the effects of prolon ged hyperkalemic cardioplegic arrest under normothermic or hypothermic conditions with respect to left ventricular myocyte contractile perfo rmance and beta-adrenergic responsiveness. Methods. Isolated left vent ricular porcine myocytes were randomly assigned to one of three groups : (group 1) normothermic control, (group 2) hypothermic cardioplegic a rrest, or (group 3) normothermic cardioplegic arrest. Myocyte contract ility was evaluated by high-speed video microscopy at baseline and aft er beta-adrenergic stimulation with isoproterenol (25 nmol/L). Results . Myocyte velocity of shortening was decreased after both hypothermic and normothermic cardioplegic arrest (68 +/- 2 and 69 +/- 2 mu m/s, re spectively) compared with normothermic control values (96 +/- 2 mu m/s ; p < 0.05). This relative reduction in baseline contractile function was equivalent in both cardioplegia groups (p = 0.5356). With beta-adr energic stimulation, myocyte velocity of shortening was 186 +/- 4 mu m /s in the hypothermic and 176 +/- 3 mu m/s in the normothermic cardiop legia groups (p = 0.0563), However, myocyte contractility with beta-ad renergic stimulation was reduced in both cardioplegia groups compared with normothermic controls (205 +/- 4 mu m/s; p < 0.05, respectively). Conclusions. Hyperkalemic cardioplegic arrest under either normotherm ic or hypothermic conditions resulted in an equivalent reduction in ba seline myocyte contractile function with reperfusion/rewarming. Hypoth ermic cardioplegic arrest may have provided mild protective effects on beta-adrenergic responsiveness. Nevertheless, these results suggest t hat an important contributory factor for diminished myocyte contractil ity after simulated cardioplegic arrest was prolonged exposure to a hy perkalemic environment. (C) 1998 by The Society of Thoracic Surgeons.