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J Thorac Cardiovasc Surg 2003;126:1880-1885
© 2003 The American Association for Thoracic Surgery

Cardiopulmonary support and physiology

Subcellular distribution of protein kinase C isozymes during cardioplegic arrest

ivojin S. Jonjev, MS, MD^a,b, Dorie W. Schwertz, PhD^c, Jennifer M. Beck, BS^c, James D. Ross, BA^c, William R. Law, PhD^a,b,*

^a Research Service, West Side Veterans Administration Medical Center, Chicago, Ill, USA
^b Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Ill, USA
^c Department of Surgical Nursing, University of Illinois at Chicago, Chicago, Ill, USA

Received for publication February 28, 2003; revisions received June 13, 2003; accepted for publication July 10, 2003.

^* Address for reprints: William R. Law, PhD, University of Illinois at Chicago, Department of Physiology and Biophysics (MC 901), 835 S Wolcott Ave, Chicago, IL 60612-7342, USA
wrlaw{at}uic.edu

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°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 , , , and were examined after separation by electrophoresis, immunoblotting/chemiluminescence, and densitometry.

RESULTS: A significant increase in protein kinase C- in the P1 fraction was detected after 5 minutes of cardioplegic arrest and remained increased for 60 minutes. Increases in P1 protein kinase C- and - were seen transiently at 5 minutes, and protein kinase C- demonstrated a secondary increase in P1 at 30 to 60 minutes. There was also a significant relative increase in protein kinase C- and protein kinase C- 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.

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