Dichloroacetate reduces plasma lactate levels but does not reduce infarct size in rabbit myocardium

Reinhard Haessler, Richard F. Davis, Roger A. Wolff, Koh Kuzume, Robert Shangraw, Donna M. Van Winkle

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

Dichloroacetate (DCA), an activator of pyruvate dehydrogenase (PDHC), enhances postischemic mechanical recovery of isolated hearts. It is not known whether this is secondary to reduced infarction or preservation of contractile function in viable cardiomyocytes. This study investigated the effect of DCA on myocardial infarct size. Anesthetized open chest rabbits underwent regional coronary occlusion and reperfusion. DCA (300 mg/kg plus 150 mg/kg 1 h later) was administered intravenously either before occlusion (DCA-O; n = 8) or at reperfusion (DCA-R; n = 7). Control rabbits (n = 8) received saline vehicle. Myocardial PDHC activity was measured after administration of 300 mg/kg i.v. DCA in 10 separate rabbits. DCA reduced plasma lactate levels and increased PDHC activity by 76%, from 2.79 ± .30 μmol/minK·g-1 to 4.92 ± .44 μmol/min·g-1 (p < .005). However, infarct size in DCA-treated animals was not significantly different from Control (60 ± 5% DCA-O, 57 ± 6% DCA-R, 58 ± 7% Control). We conclude that stimulation of pyruvate dehydrogenase does not limit infarct size.

Original languageEnglish (US)
Pages (from-to)66-71
Number of pages6
JournalShock
Volume5
Issue number1
DOIs
StatePublished - Jan 1 1996

ASJC Scopus subject areas

  • Emergency Medicine
  • Critical Care and Intensive Care Medicine

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