Normothermic versus hypothermic hyperkalemic cardioplegia: effects on myocyte contractility

This study was designed to determine the effects of prolonged hyperkalemic cardioplegic arrest under normothermic or hypothermic conditions with respect to left ventricular myocyte contractile performance and beta-adrenergic responsiveness.

Isolated left ventricular porcine myocytes were randomly assigned to one of three groups: (group 1) normothermic control, (group 2) hypothermic cardioplegic arrest, or (group 3) normothermic cardioplegic arrest. Myocyte contractility was evaluated by high-speed video microscopy at baseline and after beta-adrenergic stimulation with isoproterenol (25 nmol/L).

Myocyte velocity of shortening was decreased after both hypothermic and normothermic cardioplegic arrest (68 +/- 2 and 69 +/- 2 microns/s, respectively) compared with normothermic control values (96 +/- 2 microns/s; p < 0.05). This relative reduction in baseline contractile function was equivalent in both cardioplegia groups (p = 0.5356). With beta-adrenergic stimulation, myocyte velocity of shortening was 186 +/- 4 microns/s in the hypothermic and 176 +/- 3 microns/s in the normothermic cardioplegia groups (p = 0.0563). However, myocyte contractility with beta-adrenergic stimulation was reduced in both cardioplegia groups compared with normothermic controls (205 +/- 4 microns/s; p < 0.05, respectively).

Hyperkalemic cardioplegic arrest under either normothermic or hypothermic conditions resulted in an equivalent reduction in baseline myocyte contractile function with reperfusion/rewarming. Hypothermic cardioplegic arrest may have provided mild protective effects on beta-adrenergic responsiveness. Nevertheless, these results suggest that an important contributory factor for diminished myocyte contractility after simulated cardioplegic arrest was prolonged exposure to a hyperkalemic environment.