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Related Experiment Videos

Changes in ventricular repolarization during acidosis and low-flow ischemia

H W Bethell1, J I Vandenberg, G A Smith

  • 1Section of Cardiovascular Biology, Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom.

The American Journal of Physiology
|July 31, 1998
PubMed
Summary

Myocardial ischemia alters heart electrical activity. Acidosis, not ATP levels, activates ATP-sensitive potassium channels, shortening action potential duration during ischemia.

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Acta physiologica (Oxford, England)·2016

Area of Science:

  • Cardiology
  • Electrophysiology
  • Metabolic Research

Background:

  • Myocardial ischemia, a metabolic insult, significantly impacts cardiac mechanical and electrical function.
  • Understanding the metabolic underpinnings of electrophysiological changes during ischemia is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the metabolic contributions to electrophysiological alterations during low-flow myocardial ischemia.
  • To determine the role of intracellular pH and ATP levels in modulating cardiac ATP-sensitive potassium (KATP) channels.

Main Methods:

  • Utilized 31P NMR spectroscopy for metabolic monitoring in Langendorff-perfused ferret hearts.
  • Measured epicardial monophasic action potentials and 86Rb efflux to assess electrophysiological changes and K+ channel activity.

Related Experiment Videos

  • Induced acidosis using lactate and altered PCO2 to study its effect on action potential duration and KATP channel activity.

    • Main Results:

    • Low-flow ischemia shortened action potential duration (APD90) and increased 86Rb efflux, effects inhibited by KATP channel blockers.
    • These changes occurred with a significant fall in intracellular pH (pHi) but no change in intracellular ATP concentration ([ATP]i).
    • Both metabolic and respiratory acidosis initially lengthened APD90, followed by shortening, which was blunted by KATP channel blockade, indicating acidosis-induced KATP channel activation.

    Conclusions:

    • Intracellular acidosis, rather than altered ATP levels, is the primary metabolic driver for activating cardiac KATP channels during ischemia.
    • Lactate does not appear to have an independent metabolic effect on action potential repolarization during acidosis.
    • Findings highlight the critical role of pH in regulating cardiac electrophysiology under ischemic conditions.