Cardioprotective, inotropic and chronotropic effects of ischemic postconditioning on the model of isolated rat heart

In the experiments on the isolated perfused rat heart an effect of global ischemia (45 min) and reperfusion (30 min) on the left ventricular developed pressure (LVDP), heart rate (HR) end diastolic pressure (EDP) were estimated. Cell damage was estimated by creatine kinase release to perfusion solution. The following models of postconditioning were used: (1) three cycles of 10 s reperfusion and 10 s ischemia (RI), total cycle duration was 20 s; (2) six cycles of 10 s reperfusion and 10 s ischemia, total cycle duration was 20 s; (3) three cycles of 20 s reperfusion and 20 s ischemia, total cycle duration was 40 s; (4) six cycles of 20 s reperfusion and 20 s ischemia, total cycle duration was 40 s; (5) three cycles of 30 s reperfusion and 30 s ischemia, total cycle duration was 60 s. It was found that only postconditioning with total cycle duration 40 s or 60 s prevents an appearance of reperfusion injury of cardiomyocytes. The use of some cycles of RI with duration of 20 s has no effect on LVDP, but induces a decrease in EDP during the whole reperfusion period. Postconditioning by three cycles of RI of 40 s promoted a recovery of LVDP in reperfusion but did not affect EDP and delayed the recovery of HR. Six cycles of RI of 40 s has no effect on LVDP and EDP, but counteracts a recovery of HR in reperfusion period. Postconditioning by three cycles of RI of 60 s promotes an elevation in LVDP, decreases contracture but these effects are transient and are accompanied by the delay of recovery of HR.