It has been demonstrated that ischemic preconditioning(IP, repetitive brief period of ischemia and reperfusion) enhances recovery of post-ischemic contractile dysfunction and reduces incidences of reperfusion-arrhythmia and infarct size after a prolonged ischemia. A lot of mechanisms have been proposed, however, controversies still remain. Recent studies suggested that IP could activate protein kinase C(PKC). Therefore, we measured left ventricular function, myocardial creatinin and PKC activities, and infarct size to assess whether IPs cardioprotective effect is related to PKC activation using isolated rabbit hearts.

Hearts isolated from New Zealand White rabbits(1.5-2.0kg body weight) were perfused with Tyrode solution by Langendorff technique. After stabilization of baseline hemodynamics, the hearts were subjected to 60-min ischemia followed by 120-min reperfusion with IP(IP group, n=15) or without IP(control group, n=14), IP was induced by 4 cycles of 5-min global ischemia and 5-min reperfusion. Left ventricular function including developed pressure(LVEDP), dp/dt, heart rate(HR), and coronary flow(CF) was measured to determine the recovery of LVEDP, RPP(rate-pressure product, HRXLVEDP) and CF to baseline measurement. Frequency of arrhythmia was counted on reperfusion. Myocardial CK-MB, myocardial cytosolic and membrance PKC were measured and the infarct size was determined by staining with tetrazolium salt and planimetry. Data were analyzed by one-way ANOVA, Tukey's post-hoc test and t-test. There was no significant differences in the recovery of LVEDP, dp/dt, RPP, and CF and frequency of arrhythmia during reperfusion between the control and the IP groups. In comparison with the control groups, however, CK-MB was significantly lowered in the IP group(P < 0.05). Cytosolic PKC was significantly decreased but membrance PKC was increased(p < 0.05). These findings indicate that PKC was translocated and activated by IP. Furthermore infarct size was smaller and limited to the antero-lateral or posterior wall and papillary muscle in the IP group(p < 0.05).

These results indicate that IP dose not improve post-ischemic contractile dysfunction after a prolonged ischemia of 60 minutes but has an infarct-limiting effect. This cardioprotective effect of IP may be related to PKC activation.