THE DIRECT EFFECTS OF PROPOFOL ON MYOCYTE CONTRACTILE FUNCTION AFTER HYPOTHERMIC CARDIOPLEGIC ARREST

Propofol is being used more often in cardiac surgery, particularly aft er hypothermic, hyperkalemic cardioplegic arrest (HHCA). The purpose o f this study was to examine the effects of propofol on isolated myocyt e contractile function under both normothermic conditions and after si mulated HHCA and rewarming. Myocytes were isolated from the left ventr icle of eight pigs. Myocyte contractile function was measured under bo th normothermic conditions and after simulated HHCA (incubation at 4 d egrees C for 2 h in crystalloid cardioplegia; K+=24 mEq/L) using compu ter-assisted videomicroscopy in the presence of 2, 4, and 6 mu g/mL pr opofol (11.2, 22.4, and 33.6 mu M/L, respectively). Isoproterenol (25 nM) was then added and contractile function measurements repeated. Pro pofol caused significant dose-dependent reductions in myocyte velocity of shortening (baseline=67+/-2 mu m/s; propofol=2 mu g/mL, 45+/-4 mu m/s; and propofol=6 mu g/mL, 27+/-3 mu m/s; P <0.05). HHCA and rewarmi ng caused a significant reduction in myocyte velocity of shortening (2 9+/-0.9 mu m/s, P <0.05), with further significant dose-dependent redu ctions in contractile function after the addition of propofol. Propofo l caused a decrease in beta-adrenergic responsiveness under normotherm ic conditions, but not after simulated HHCA. Results from the present study demonstrated for the first time that the reduction in isolated m yocyte contractile function after simulated HHCA is further decreased by propofol administration.