Catecholamine-induced heart injury in mice: differential effects of isoproterenol and phenylephrine

Míriam Navarro-Sobrino1, Jordi Lorita, Maria Soley

  • 1Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona, Barcelona, Spain.

Insights

Acute stress can injure the heart, but receptor roles are unclear. Alpha1-adrenergic receptors primarily cause catecholamine-induced heart injury, while beta-adrenergic receptors mediate beneficial effects.

Area of Science:

  • Cardiovascular Physiology
  • Pharmacology
  • Stress Response

Background:

  • Catecholamines are involved in stress-induced heart injury.
  • The specific roles of different adrenergic receptor types in this process are not fully understood.

Purpose of the Study:

  • To investigate the contribution of alpha1- and beta-adrenergic receptors to catecholamine-induced heart injury and function.
  • To compare the effects of phenylephrine (alpha1 agonist) and isoproterenol (beta agonist) on cardiac markers and tissue damage.

Main Methods:

  • Comparison of plasma enzyme activities (LDH-1, AST) and cardiac lesion morphology in adrenaline-injected mice versus stressed mice.
  • Langendorff-perfused rat heart experiments to assess adrenergic receptor contributions to heart rate and contractility.
  • Administration of phenylephrine and isoproterenol to whole mice to evaluate their effects on cardiac markers and myocardial tissue.

Main Results:

  • Phenylephrine, but not isoproterenol, increased cardiac enzyme activities (LDH-1, AST) in whole mice.
  • Phenylephrine-injected hearts exhibited necrotic lesions and leukocyte infiltration, whereas isoproterenol-injected hearts showed fewer necrotic areas.
  • Alpha1-adrenergic receptors played a minor role in the tonic effects of adrenaline on heart rate and contractility in perfused rat hearts.

Conclusions:

  • The cardiotonic effects of catecholamines are mediated primarily by beta-adrenergic receptors.
  • Acute catecholamine-induced heart injury is mainly mediated by alpha1-adrenergic receptors.

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