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We tested recent evidence that ischemic preconditioning (PC) involves in translocation of protein kinase C (PKC) from the cytosol to myocyte membrane. Isolated Langendorff-perfused rabbit hearts (n=96) were subjected to 60 or 45 min of ischemia (I) and 120 min of reperfusion (R) with or without PC (4 cycles of 5 min I and 5 min R; or single dose of 5 min I and 10 min R), respectively. Left ventricular function and infarct size (IS) were measured; myocardial cytosolic and membrane PKC activity were determined by 32P-gamma-ATP incorporation into PKC-specific peptide. PC enhanced improvement of functional recovery and reduced IS (26.9+/-1.4% versus 15.3+/-1.9%, p&lt;0.01, in 60 min of I; 18.3+/-2.6% versus 8.6+/-2.5%, p&lt;0.05, in 45 min of I); cytosolic PKC activity decreased 74% of total activity (p&lt;0.05) both in 60 and 45 min of I; membrane PKC activity increased (1.7-fold of baseline, p&lt;0.01, in 60 min of I; 1.8-fold, p&lt;0.01, in 45 min of I; 1.5-fold, p&lt;0.05, in 60 of min I and 120 min of R). From these results, it is concluded that translocation of PKC from the cytosol to myocyte membranes is an important mechanism responsible for PC effect.

Evidence of protein kinase C translocation by ischemic preconditioning in global ischemia model