VENTRICULAR OVERDRIVE PACING-INDUCED PRECONDITIONING AND NO-FLOW ISCHEMIA-INDUCED PRECONDITIONING IN ISOLATED WORKING RAT HEARTS

To examine preconditioning induced by short periods of ventricular ove rdrive pacing (VOP) as compared with that induced by no-flow ischemia, we subjected isolated working rat heart to 10-min coronary artery occ lusion (test ischemia) followed by 3-min reperfusion after three inter mittent periods of VOP (10 Hz) or 5-min no-flow ischemia, respectively . In the nonpreconditioned group, coronary occlusion decreased aortic flow (AF) from 46.6 +/- 2.4 to 13.7 +/- 1.7 ml/min and increased left ventricular end-diastolic pressure (LVEDP) from 0.53 +/- 0.05 to 2.02 +/- 0.07 kPa. Preconditioning by VOP or no-flow ischemia significantly increased AF to 25.1 +/- 2.3 ml/min (p < 0.001) and to 27.3 +/- 1.4 m l/min (p < 0.001) and decreased LVEDP to 1.38 +/- 0.1 kPa (p < 0.001) and to 1.65 +/- 0.05 kPa (p < 0.05), respectively, after test ischemia . Glibenclamide 10(-7) M which blocked the antiischemic effect of the ATP-sensitive K+-channel (K-ATP) opener cromakalim, inhibited VOP-indu ced protection (AF 20.3 +/- 2.3 ml/min; LVEDP 1.82 +/- 0.15 kPa), but did not affect no-flow ischemia-induced preconditioning [AF 26.6 +/- 2 .4 ml/min (p < 0.001), LVEDP 1.60 +/- 0.07 kPa (p < 0.01)]. VOP and no -flow ischemia precondition heart, however their cardioprotective mech anisms may be different in terms of K-ATP activation in rats.