Decreased intracellular pH is not due to increased H+ extrusion in preconditioned rat hearts

Scott A. Gabel, Heather R. Cross, Robert E. London, Charles Jr Steenbergen, Elizabeth Murphy

Research output: Contribution to journalArticle

Abstract

Ischemic precondition-ing reduces intracellular acidification during a subsequent, prolonged period of ischemia. This may reflect decreased anaerobic glycolysis or increased H+ efflux. To distinguish between these hypotheses, we monitored intracellular and extracellular pH during a sustained period of ischemia to determine whether the preconditioned hearts had increased H+ efflux compared with nonpreconditioned hearts. At the end of 20 min of ischemia, intracellular pH in nonpreconditioned hearts was 5.90 ±0.08 and extracellular pH was 5.51 ±0.21, whereas in preconditioned hearts, intracellular pH was 6.50 ±0.06 and extracellular pH was 6.62 ±0.06. To investigate whether an Na+/H+ exchange inhibitor would alter the reduced acidification during ischemia, we preconditioned hearts with and without dimethylamiloride (DMA). Intracellular pH during ischemia was similar in preconditioned hearts with and without DMA treatment (pH 6.42 ± 0.02 vs. 6.45 ±0.03, respectively). These data do not support the hypothesis that enhanced proton efflux is responsible for the more alkaline intracellular pH during sustained ischemia in preconditioned hearts.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume42
Issue number5
StatePublished - 1997
Externally publishedYes

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Ischemia
Glycolysis
Protons
5-dimethylamiloride

Keywords

  • Phosphorus-31 nuclear magnetic resonance
  • Preconditioning

ASJC Scopus subject areas

  • Physiology

Cite this

Decreased intracellular pH is not due to increased H+ extrusion in preconditioned rat hearts. / Gabel, Scott A.; Cross, Heather R.; London, Robert E.; Steenbergen, Charles Jr; Murphy, Elizabeth.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 42, No. 5, 1997.

Research output: Contribution to journalArticle

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