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

Background: We have previously demonstrated, in the isolated rat heart, that propofolattenuates hydrogen peroxide-induced damage and ischaemia- reperfusion injury, and that the beneficial effect of propofolis correlated with reduction of the lipid peroxidation. This study was designed to evaluate whether propofolhas a cardioprotectiveeffect against ischaemia- reperfusion injuryin a rat model in vivo. Methods: Adult rats were anaesthetized with pentobarbital10mg kg -1 h -1 alone (control group), pentobarbital10 or 20 mg kg -1 h -1 + Intralipid® as a vehicle (Pent-10, Pent-20 group), propofol10 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 malondialdehydewas 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 malondialdehydein 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 propofolcould be cardioprotectiveagainst ischaemia- reperfusion injurydose dependently in a rat model in vivo and that the beneficial action of propofolmay be correlated with its antioxidant effect.