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Circulation. 2003 Nov 11;108(19):2304-7. Epub 2003 Nov 3.

Inhibition of delta-protein kinase C protects against reperfusion injury of the ischemic heart in vivo.

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1
Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, Calif 94305-5174, USA.

Abstract

BACKGROUND:

Current treatment for acute myocardial infarction (AMI) focuses on reestablishing blood flow (reperfusion). Paradoxically, reperfusion itself may cause additional injury to the heart. We previously found that delta-protein kinase C (deltaPKC) inhibition during simulated ischemia/reperfusion in isolated rat hearts is cardioprotective. We focus here on the role for deltaPKC during reperfusion only, using an in vivo porcine model of AMI.

METHODS AND RESULTS:

An intracoronary application of a selective deltaPKC inhibitor to the heart at the time of reperfusion reduced infarct size, improved cardiac function, inhibited troponin T release, and reduced apoptosis. Using 31P NMR in isolated perfused mouse hearts, we found a faster recovery of ATP levels in hearts treated with the deltaPKC inhibitor during reperfusion only.

CONCLUSIONS:

Reperfusion injury after cardiac ischemia is mediated, at least in part, by deltaPKC activation. This study suggests that including a deltaPKC inhibitor at reperfusion may improve the outcome for patients with AMI.

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