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Updated: Aug 29, 2026
Murine Isolated Heart Model of Myocardial Stunning Associated with Cardioplegic Arrest
Published on: August 6, 2015
Subcellular distribution of protein kinase C isozymes during cardioplegic arrest
Zivojin S Jonjev1, Dorie W Schwertz, Jennifer M Beck
1Research Service, West Side Veterans Administration Medical Center, Chicago, IL, USA.
Background:
On the basis of the hypothesis that cardioplegia-associated myocardial depression was due to activation of protein kinase C, we examined whether specific protein kinase C isozymes would translocate to a cellular fraction containing myofilaments.
Methods:
Isolated rat hearts were perfused with Krebs-Ringer bicarbonate buffer for 30 minutes and arrested with 4 degrees C St Thomas No. 2 cardioplegic solution for 0 to 120 minutes (n = 5 per group). The 3 fractions of the left ventricle tissue represented the myofibrillar/nuclear fraction (P1), membranes (P2), and cytosol (supernatant). The distributions of protein kinase C isozymes alpha, delta, epsilon, and eta were examined after separation by electrophoresis, immunoblotting/chemiluminescence, and densitometry.
Results:
A significant increase in protein kinase C-delta in the P1 fraction was detected after 5 minutes of cardioplegic arrest and remained increased for 60 minutes. Increases in P1 protein kinase C-alpha and -epsilon were seen transiently at 5 minutes, and protein kinase C-epsilon demonstrated a secondary increase in P1 at 30 to 60 minutes. There was also a significant relative increase in protein kinase C-alpha and protein kinase C-delta in the P2 fraction after 60 minutes of cardioplegia.
Conclusions:
These data are consistent with our hypothesis that activation of protein kinase C isozymes is associated with altered myofilament function after cardioplegic arrest.
