Abstract
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-γ-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<0.01, in 60 min of I;
18.3±2.6% versus 8.6±2.5%, p<0.05, in 45 min of I); cytosolic PKC activity
decreased 74% of total activity (p<0.05) both in 60 and 45 min of I; membrane
PKC activity increased (1.7-fold of baseline, p<0.01, in 60 min of I; 1.8-fold,
p<0.01, in 45 min of I; 1.5-fold, p<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.