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Extracellular magnesium and cardiotonic steroid toxicity in isolated myocardial preparations

R Kafiluddi1, R H Kennedy, E Seifen

  • 1Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock.

Insights

Extracellular magnesium (Mg++0) reduces sensitivity to cardiotonic steroid-induced arrhythmias in guinea pig hearts. This effect is not due to changes in receptor binding or Na+-pump activity.

Area of Science:

  • Cardiovascular Physiology
  • Pharmacology
  • Biochemistry

Background:

  • Cardiotonic steroids (e.g., digoxin) are used to treat heart failure.
  • Their therapeutic use is limited by toxic side effects, including arrhythmias.
  • Extracellular magnesium (Mg++0) is a critical ion in cardiac function.

Purpose of the Study:

  • To investigate the direct effects of extracellular magnesium (Mg++0) on the positive inotropic and toxic actions of cardiotonic steroids.
  • To determine the mechanisms underlying Mg++0's influence on cardiotonic steroid toxicity.

Main Methods:

  • Isolated guinea pig left atrial muscle preparations were used to assess inotropic and arrhythmogenic effects.
  • Experiments were conducted using partially purified membrane preparations to study [3H]ouabain binding and Na+,K+-adenosine triphosphatase activity.
  • Fractional occupancy estimates were used to evaluate receptor binding levels.

Main Results:

  • Increased Mg++0 concentrations demonstrated a negative inotropic effect and reduced sensitivity to digoxin-induced arrhythmias.
  • Mg++0 did not alter maximum developed tension before dysrhythmic activity or affect contracture sensitivity.
  • Elevated Mg++ enhanced affinity for [3H]ouabain in membrane preparations but did not affect binding site density or Na+-pump activity in intact tissue.

Conclusions:

  • Extracellular magnesium (Mg++0) directly antagonizes cardiotonic steroid-induced arrhythmias in the myocardium.
  • The observed protective effect of Mg++0 is likely mediated by altered responsiveness rather than changes in receptor binding or Na+-pump capacity.

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