Literature DB >> 14597593

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

Koichi Inagaki1, Leon Chen, Fumiaki Ikeno, Felix H Lee, Ken-ichi Imahashi, Donna M Bouley, Mehrdad Rezaee, Paul G Yock, Elizabeth Murphy, Daria Mochly-Rosen.   

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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Year:  2003        PMID: 14597593     DOI: 10.1161/01.CIR.0000101682.24138.36

Source DB:  PubMed          Journal:  Circulation        ISSN: 0009-7322            Impact factor:   29.690


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