Electrophysiologic effects of selective B1 adrenergic stimulation in the late phase of myocardial infarct healing.
Nonspecific adrenergic stimulation plays an important role in the genesis of ventricular tachyarrhythmias in the postinfarction period. However, the role of selective B1 adrenergic stimulation in the aggravation of reentrant ventricular tachycardia is still poorly understood. The purpose of this investigation was to study the regional electrophysiologic actions and arrhythmogenic effects of the B1 adrenergic agonist dobutamine in a postinfarction canine model. Eleven dogs with 4-week-old anterior wall myocardial infarctions, chronic indwelling intramyocardial electrodes and no inducible sustained ventricular tachycardia at baseline, were studied in the closed-chest state at baseline (control) and during intravenous infusion of dobutamine 10 micrograms/kg/min. Dobutamine caused reductions in the effective and absolute refractory periods in the infarct, peri-infarct and noninfarcted regions of the myocardium which were similar in magnitude at each region. With dobutamine, only 1 dog had inducible sustained ventricular tachycardia (polymorphic). No spontaneous arrhythmias were seen. In summary, selective B1 adrenergic stimulation alone does not cause dispersion of myocardial refractoriness and does not cause significant proarrhythmia in the chronically infarcted canine heart. Additional metabolic, electrolyte or ischemic abnormalities may be required for B1 adrenergic stimulation to aggravate arrhythmias in this model.
Nelson
S D
SD
Division of Cardiology, Ohio State University, Columbus.
Coyne
K
K
D000818:Animals; D004195:Disease Models, Animal; D004280:Dobutamine / Q000494:pharmacology*; D004285:Dogs; D006329:Heart Conduction System / Q000187:drug effects*; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D013610:Tachycardia / Q000503:physiopathology
D004280:Dobutamine