Although ischemic preconditioning (IPC) or propofol is generally known to confer the cardioprotective effect on ischemic-reperfused hearts, especially in patients subjected to operation such as cardiopulmonary bypass and heart transplantation, the exact effects of IPC and propofol are still controversial. Furthermore, the interaction between IPC- and propofol-induced cardioprotective effects has not been studied yet. The aims of this study are to examine 1) whether IPC and propofol demonstrates the cardioprotective effect against ischemic-reperfusion injury in the isolated rat hearts, and if so, 2) whether the combination of IPC and propofol shows the additive effects.

Isolated rat hearts were subjected to 30 min global ischemia followed by 60 min of reperfusion. Four groups of hearts (n = 7 per group) were studied. Group control (no intervention); group IPC, two 2-min total coronary occlusions (ischemic preconditioning) interspersed with 5 min and 6 min of normal perfusion before global ischemia; group propofol, propofol 2 µg/ml (11.1 µM) administered before global ischemia and during reperfusion; group propofol/IPC, propofol 2 µg/ml administered before IPC and during reperfusion. Left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), + dP/dt_max and - dP/dt_min were recorded and creatinine kinase (CK) in coronary effluent perfusate and coronary flow also were measured.

There were significant differences in recovery of postischemic systolic function between control and IPC, propofol and propofol/IPC as assessed by LVDP, expressed as a percentage of preischemic value (22.2 ± 8.4 vs 59.4 ± 6.8, 69.4 ± 7.9 and 66.0 ± 7.1%, respectively; P < 0.05) at the end of reperfusion. The propofol and propofol/IPC showed better recovery in postischemic relaxation than IPC or control as asse ssed by LVEDP (11.3 ± 2.2 and 11.3 ± 6.1 vs 56 ± 6.0 or, 25.2 ± 7.6 mmHg, respectively; P < 0.05). There were significant differences in attenuation of myocardial damage between propofol/IPC and control as assessed by % change of CK (135.5 ± 54.7 vs 602.3 ± 225.1%, P < 0.05) and % change of coronary flow (66.6 ± 4.0 vs 39.2 ± 5.2%, P < 0.05).

These results suggest that ischemic preconditioning combined with propofol may not show any additive effect on IPC-and propofol-induced attenuation of postischemic ventricular dysfunction, however it show the tendency to attenuate the myocardial damage.