Propofol attenuates ischaemia-reperfusion injury in the rat heart in vivo.

Background: We have previously demonstrated, in the isolated rat heart, that propofol attenuates hydrogen peroxide-induced damage and ischaemia-reperfusion injury, and that the beneficial effect of propofol is correlated with reduction of the lipid peroxidation. This study was designed to evaluate whether propofol has a cardioprotective effect against ischaemia-reperfusion injury in a rat model in vivo. Methods: Adult rats were anaesthetized with pentobarbital 10mg kg -1 h -1 alone (control group), pentobarbital 10 or 20 mg kg -1 h -1 + Intralipid® as a vehicle (Pent-10, Pent-20 group), propofol 10 or 20 mg kg -1 h -1 (Prop-10, Prop-20 group) intravenously throughout the experiment. The left anterior descending coronary artery was occluded for 30 min followed by 120 min of reperfusion. Infarct size was determined at the end of reperfusion. The tissue concentration of malondialdehyde was measured at 30 min after reperfusion to evaluate lipid peroxidation. Results: The infarct sizes (% of area at risk) were significantly smaller in the Prop-10 (54 ± 11%; P<0.01 vs. control) and Prop-20 (39 ± 8%; P < 0.01 vs. control) groups than in the control (68 ± 9%), Pent-10 (69 ±13%) and Pent-20 (68 ± 14%) groups (n = 12). In the Pent-10 and Pent-20 groups, ischaemia-reperfusion produced significant increases in the values for tissue malondialdehyde (0.72 ± 0.24 μmol mgprotein -1 ; P< 0.05 and 0.63 ± 0.33 μmol mg protein -1 ; P<0.05 vs. 0.46 ± 0.22 μmol mg protein -1 in non-ischaemic hearts, n = 8). However, the values of malondialdehyde in the Prop-10 and -20 groups were suppressed by 41% and 63%, respectively, compared with the Pent-10 group (P < 0.01). Conclusion: Our results suggest that propofol could be cardioprotective against ischaemia-reperfusion injury dose dependently in a rat model in vivo and that the beneficial action of propofol may be correlated with its antioxidant effect.