Fig. 2. Hemodynamic changes in hearts subjected to ischemia or reperfusion. The functional improvement by anesthetic preconditioning (APC ) and ischemic preconditioning (IPC ) was completely abolished by the protein kinase C (PKC ) inhibitors chelerythrine (CHE ) and rottlerin (ROT ) as well as by the mitochondrial K^ATP(mitoK^ATP) channel blocker 5-hydroxydecanoate (5HD), albeit at different concentrations. IPC and APC were not blocked by HMR-1098. Effects of chelerythrine and rottlerin in APC (A ) and IPC (B ). Effects of 5HD and HMR-1098 in APC (C ) and IPC (D ). Numbers behind individual blockers indicate concentrations in μm. Values are mean ± SEM (n = 7 for each group). For comparisons between groups during the treatment period and the effects of the blockers alone on postischemic functional improvement, see table 1. CTL = control, EDP = end-diastolic pressure, sarcK^ATP= sarcolemmal K^ATP.