OBJECTIVE: To examine whether propofol protects against postischemic myocardial dysfunction and apoptosis during reperfusion after prolonged cold ischemia in isolated rat hearts. DESIGN: A prospective, randomized, controlled study. SETTING: A university laboratory. PARTICIPANTS: Animals. INTERVENTIONS: The isolated hearts of 40 Sprague-Dawley male rats were perfused with modified Krebs-Hennseleit solution for 15 minutes for a stabilization period and 15 minutes for a perfusion period and then underwent 4 hours of global cold ischemia followed by 60 minutes of reperfusion. Four groups were studied (n = 10 for each group). Ten hearts served as an untreated control group. Propofol (2 micromol/L) treatment was performed only before ischemia in the PRE group, only during reperfusion in the POST group, and both before and after ischemia in the ALL group. MEASUREMENTS AND MAIN RESULTS: Infusion of propofol during reperfusion improved recovery of left ventricular-developed pressure (LVDP) from 61.2% +/- 8.5% (control) to 86.3% +/- 12.1% (POST) and 74.9% +/- 13.2% (ALL, both p < 0.05), whereas preischemic infusion of propofol (64.3% +/- 9.7%, PRE) did not improve recovery of LVDP. Infusion of propofol during reperfusion significantly reduced the number of apoptotic cells and led to a smaller infarct size than control and PRE groups (p < 0.05, respectively). CONCLUSIONS: Propofol infusion during the reperfusion period produced a cardioprotective effect and inhibited apoptosis of cardiomyocytes in the ischemia-reperfusion model, with prolonged cold ischemia, in isolated rat hearts.
OBJECTIVE: To examine whether propofol protects against postischemic myocardial dysfunction and apoptosis during reperfusion after prolonged cold ischemia in isolated rat hearts. DESIGN: A prospective, randomized, controlled study. SETTING: A university laboratory. PARTICIPANTS: Animals. INTERVENTIONS: The isolated hearts of 40 Sprague-Dawley male rats were perfused with modified Krebs-Hennseleit solution for 15 minutes for a stabilization period and 15 minutes for a perfusion period and then underwent 4 hours of global cold ischemia followed by 60 minutes of reperfusion. Four groups were studied (n = 10 for each group). Ten hearts served as an untreated control group. Propofol (2 micromol/L) treatment was performed only before ischemia in the PRE group, only during reperfusion in the POST group, and both before and after ischemia in the ALL group. MEASUREMENTS AND MAIN RESULTS: Infusion of propofol during reperfusion improved recovery of left ventricular-developed pressure (LVDP) from 61.2% +/- 8.5% (control) to 86.3% +/- 12.1% (POST) and 74.9% +/- 13.2% (ALL, both p < 0.05), whereas preischemic infusion of propofol (64.3% +/- 9.7%, PRE) did not improve recovery of LVDP. Infusion of propofol during reperfusion significantly reduced the number of apoptotic cells and led to a smaller infarct size than control and PRE groups (p < 0.05, respectively). CONCLUSIONS:Propofol infusion during the reperfusion period produced a cardioprotective effect and inhibited apoptosis of cardiomyocytes in the ischemia-reperfusion model, with prolonged cold ischemia, in isolated rat hearts.