Key result
Myocardial infarction provoked an enhanced beta2-adrenergic receptor contractile response in dogs susceptible to ventricular fibrillation, but not in resistant animals.
Why the study?
Does beta-AR stimulation elicit different contractile responses in dogs susceptible vs resistant to lethal arrhythmias before and after myocardial infarction?
Population
Dogs susceptible or resistant to ventricular fibrillation induced by a 2-min coronary occlusion during the…
Comparison
Isoproterenol with or without beta1-AR… vs Baseline vs after infarction; Susceptible vs…
Design
Preclinical
Authors
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May inform beta2-AR targeting in post-MI arrhythmia research; hypothesis-generating in animal models and should not yet change practice.
Does beta-AR stimulation elicit different contractile responses in dogs susceptible vs resistant to lethal arrhythmias before and after myocardial infarction?
Myocardial infarction provokes an enhanced beta2-adrenergic receptor contractile response in dogs susceptible to lethal arrhythmias, suggesting a mechanism for arrhythmogenesis.
Houle et al. (2001) studied Susceptibility to ventricular fibrillation (n=27). Isoproterenol and beta-adrenergic receptor antagonists vs. Resistant dogs / before myocardial infarction was evaluated on Velocity of circumferential fiber shortening (Vcf), heart rate response, and single-cell isotonic shortening response. Myocardial infarction provoked an enhanced beta2-adrenergic receptor contractile response in dogs susceptible to ventricular fibrillation, but not in resistant animals.
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