Postischemic Function and Protein Kinase C Signal Transduction

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Manuel J. Antunes, MD, PhD, DSc

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Presentation transcript:

Postischemic Function and Protein Kinase C Signal Transduction Thomas J Rohs, MD, Kenneth S Kilgore, PhD, Anthony J Georges, MD, Steven F Bolling, MD The Annals of Thoracic Surgery Volume 65, Issue 6, Pages 1680-1684 (June 1998) DOI: 10.1016/S0003-4975(98)00232-X

Fig 1 Percent functional recovery with protein kinase C agonists/antagonists. Recovery of developed pressure (DP) is shown for all the groups and compared as a percentage of preischemic values versus 45 minutes after reflow. Hearts received either protein kinase C agonist acetylcholine (ACH), protein kinase C agonist 1,2-s,n-dioctanoylglycerol (DOG), vehicle dimethyl sulfoxide (DMSO), protein kinase C antagonist chelerythrine (CHEL), or DOG and chelerythrine, with cardioplegia alone used as controls (CTL). (Mean ± standard error of the mean; p < 0.05 for ACH and DOG versus control.) The Annals of Thoracic Surgery 1998 65, 1680-1684DOI: (10.1016/S0003-4975(98)00232-X)

Fig 2 Protein kinase C (PKC) translocation in response to protein kinase C agonists/antagonists, shown as percent of total protein kinase C at membrane. Baseline was after stabilization. Ischemic hearts were subjected to 2 hours of unprotected ischemia. DOG and Chel/DOG hearts received either the protein kinase C agonist 1,2-s,n-dioctanoylglycerol (DOG) or DOG and the protein kinase C antagonist chelerythrine (Chel), administered for 15 minutes and 25 minutes before 120 minutes of cardioplegic induced ischemia. The Annals of Thoracic Surgery 1998 65, 1680-1684DOI: (10.1016/S0003-4975(98)00232-X)