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Magnesium attenuates isoproterenol-induced acute cardiac dysfunction and beta-adrenergic desensitization

Yin-Tie Jin1, Naoyuki Hasebe, Tomoyuki Matsusaka

  • 1Dept of Internal Medicine, Division of Cardiology, Asahikawa Medical College, 2-1-1-1 Midorigaoka Higashi, Asahikawa, Hokkaido, Japan.

American Journal of Physiology. Heart and Circulatory Physiology
|November 23, 2006
PubMed

Insights

Magnesium supplementation significantly protected against isoproterenol-induced acute cardiac dysfunction in dogs. It also prevented beta-adrenergic desensitization and myocardial damage, highlighting magnesium

Area of Science:

  • Cardiology
  • Cardiovascular Physiology
  • Pharmacology

Background:

  • Sympathetic nervous system activation is vital in heart failure but excess catecholamines can harm the heart.
  • Magnesium is recognized for cardioprotective properties, yet its role in acute cardiac dysfunction needs further study.
  • Isoproterenol is used to model acute cardiac dysfunction and sympathetic overstimulation.

Purpose of the Study:

  • To investigate the protective effects of magnesium against left ventricular (LV) dysfunction induced by high-dose isoproterenol in a canine model.
  • To assess magnesium's impact on beta-adrenergic responsiveness and myocardial damage markers.

Main Methods:

  • Anesthetized dogs received continuous infusions of isoproterenol, with or without magnesium.
  • Left ventricular systolic and diastolic functions were assessed.
  • Dose-response to lower isoproterenol doses and serum markers (ionized calcium, lipid peroxide, myocardial damage) were measured.

Main Results:

  • High-dose isoproterenol impaired LV systolic function, slowed relaxation, and reduced responsiveness to isoproterenol.
  • Magnesium administration significantly mitigated isoproterenol-induced systolic and diastolic dysfunction.
  • Magnesium maintained serum ionized calcium levels, suppressed lipid peroxide elevation, and reduced myocardial damage markers.

Conclusions:

  • Magnesium effectively attenuates acute cardiac dysfunction and beta-adrenergic desensitization caused by excessive isoproterenol.
  • Magnesium demonstrates significant cardioprotective effects in the context of acute sympathetic overstimulation.
  • These findings support magnesium's potential therapeutic role in managing acute cardiac stress.

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