[Effects of ischemic preconditioning on the recovery of myocardial function after unprotected ischemia and cardioplegia in the isolated and crystalloid perfused rat hearts].

Preconditioning with repetitive brief periods of ischemic (IPC) is known to induce myocardial protection against a subsequent more prolonged period of ischemia. We investigated whether IPC can offer similar beneficial effects on myocardial function after cardioplegic preservation in isolated and crystalloid-perfused rat hearts. IPC was produced by 5 periods of 1 min ischemia followed by 5 min reperfusion before 25 min of unmodified ischemia or 40 min of cardioplegia. IPC had no significant effect on the time to contractile arrest (control: 211 +/- 27 sec, IPC: 240 +/- 32 sec) after unmodified ischemia, while the time to electrical asystole was significantly (p < 0.05) shortened by IPC (676 +/- 107 sec) compared to control (1021 +/- 197 sec). However, rapid contractile arrest concomitant with electrical asystole was induced by infusion of St. Thomas' Hospital solution in control as well as in IPC-treated hearts without a significant intergroup difference (control: 33 +/- 7 sec, IPC 39 +/- 9 sec). Although myocardial ATP was significantly reduced by IPC, IPC-treated hearts showed a significantly higher ATP level after 25 min of unprotected ischemia. Accumulation of myocardial lactate after 25 min of unprotected ischemia was significantly (p < 0.05) inhibited by IPC. However, the levels of myocardial ATP and lactate after 40 min of cardioplegia were comparable between control and IPC-treated hearts. Left ventricular developed pressure (LVDP) at 30 min reperfusion after unprotected ischemia was significantly improved by IPC, while the recovery of LVDP at 30 min reperfusion after cardioplegia was comparable between control and IPC-treated hearts. The onset of ischemic contracture, i.e., a rise of left ventricular end-diastolic pressure (LVEDP), was significantly accelerated and its magnitude was significantly greater in IPC-treated hearts during unprotected ischemia and also during cardioplegia. However, a significant decrease of LVEDP during reperfusion compared to control hearts was observed only after unprotected ischemia. The amounts of creatine kinase (CK) released during 30 min reperfusion after unprotected ischemia was significantly greater in control than in IPC-treated hearts, but there was no significant difference in CK release between control and IPC-treated hearts during reperfusion after cardioplegia. These results suggest that IPC-induced cardioprotection may be induced via inhibition of anaerobic energy metabolism through a negative chronotropic effect during unprotected ischemia, but such a beneficial effect is dissipated with cardioplegia by which rapid electrical asystole is induced. It is, therefore, concluded that IPC may not provide additional myocardial protection over conventional hyperkalemic cardioplegia.