HOE-642 (cariporide) alters pHi and diastolic function after ischemia during reperfusion in pig hearts in situ

Michael A. Portman, Anthony L. Panos, Yun Xiao, David L. Anderson, Xue Han Ning

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

The specific Na+/H+ exchange inhibitor HOE-642 prevents ischemic and reperfusion injury in the myocardium. Although this inhibitor alters H+ ion flux during reperfusion in vitro, this action has not been confirmed during complex conditions in situ. Myocardial intracellular pH (pHi) and high-energy phosphates were monitored using 31P magnetic resonance spectroscopy in openchest pigs supported by cardiopulmonary bypass during 10 min of ischemia and reperfusion. Intravenous HOE-642 (2 mg/kg; n = 8) administered before ischemia prevented the increases in diastolic stiffness noted in control pigs (n = 8), although it did not alter the postischemic peak-elastance or pressure-rate product measured using a distensible balloon within the left ventricle. HOE-642 induced no change in phi during ischemia but caused significant delays in intracellular realkalinization during reperfusion. HOE-642 did not alter phosphocreatine depletion and repletion but did improve ATP preservation. Na+/H+ exchange inhibition through HOE-642 delays intracellular alkalinization in the myocardium in situ during reperfusion in association with improved diastolic function and high-energy phosphate preservation.

Original languageEnglish (US)
Pages (from-to)H830-H834
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume280
Issue number2 49-2
DOIs
StatePublished - Feb 2001

Keywords

  • Intracellular pH
  • Magnetic resonance spectroscopy
  • Metabolism
  • Phosphates

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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