Beta2-adrenergic receptor antagonists protect against ventricular fibrillation: in vivo and in vitro evidence for enhanced sensitivity to beta2-adrenergic stimulation in animals susceptible to sudden death

Circulation. 1997 Sep 16;96(6):1914-22. doi: 10.1161/01.cir.96.6.1914.

Abstract

Background: The ventricular myocardium contains functional beta2-adrenergic receptors that when activated increase intracellular Ca2+ transients. Because elevated Ca2+ has been implicated in the induction of ventricular fibrillation (VF), it is possible that the activation of these receptors may also provoke malignant arrhythmias.

Methods and results: To test this hypothesis, a 2-minute occlusion of the left circumflex coronary artery was made during the last minute of exercise in 28 dogs with healed anterior myocardial infarctions: 17 had VF (susceptible) and 11 did not (resistant). On a subsequent day, this test was repeated after administration of the beta2-adrenergic receptor antagonist ICI 118,551 (0.2 mg/kg). This drug did not alter the hemodynamic response to the coronary occlusion, yet it prevented VF in 10 of 11 animals tested (P<.001). However, heart rate was reduced in 6 animals. Therefore, the ICI 118,551 exercise-plus-ischemia test was repeated with heart rate held constant by ventricular pacing (n=3). ICI 118,551 still prevented VF when heart rate was maintained. Next, the effects of increasing doses of the beta2-adrenergic receptor agonist zinterol on Ca2+ transient amplitudes were examined in ventricular myocytes. Zinterol elicited significantly greater increases in Ca2+ transient amplitudes at all doses tested (10(-9) to 10(-6) mol/L) in myocytes prepared from susceptible versus resistant animals. The cardiomyocyte response to isoproterenol (10(-7) mol/L) in the presence or absence of the selective beta1- (CGP-20712A, 300 nmol/L) or beta2- (ICI 118,551, 100 nmol/L) adrenergic receptor antagonist was also examined. Isoproterenol elicited larger Ca2+ transient increases in the susceptible myocytes, which were eliminated by ICI but not by CGP.

Conclusions: When considered together, these data demonstrate that canine myocytes contain functional beta2-adrenergic receptors that are activated to a greater extent in the susceptible animals. The resulting cytosolic Ca2+ transient increases may lead to afterpotentials that ultimately trigger VF in these animals.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adrenergic beta-2 Receptor Agonists
  • Adrenergic beta-2 Receptor Antagonists*
  • Adrenergic beta-Agonists / pharmacology
  • Adrenergic beta-Antagonists / pharmacology
  • Animals
  • Calcium / metabolism
  • Cells, Cultured
  • Cyclic AMP / biosynthesis
  • Death, Sudden / etiology
  • Dogs
  • Ethanolamines / pharmacology
  • Exercise Test
  • Imidazoles / pharmacology
  • Isoproterenol / pharmacology
  • Muscle Fibers, Skeletal / chemistry
  • Muscle Fibers, Skeletal / cytology
  • Muscle Fibers, Skeletal / metabolism
  • Myocardial Ischemia / complications
  • Myocardial Ischemia / mortality
  • Myocardium / chemistry
  • Myocardium / cytology
  • Myocardium / metabolism
  • Propanolamines / pharmacology
  • Sensitivity and Specificity
  • Ventricular Fibrillation / drug therapy*
  • Ventricular Fibrillation / mortality
  • Ventricular Fibrillation / prevention & control*

Substances

  • Adrenergic beta-2 Receptor Agonists
  • Adrenergic beta-2 Receptor Antagonists
  • Adrenergic beta-Agonists
  • Adrenergic beta-Antagonists
  • Ethanolamines
  • Imidazoles
  • Propanolamines
  • ICI 118551
  • zinterol
  • CGP 20712A
  • Cyclic AMP
  • Isoproterenol
  • Calcium