Adenosine deaminase and adenosine attenuate ventricular arrhythmias caused by norepinephrine

Twenty-five beagles weighing 9.1 +/- 0.4 kg were used to investigate the arrhythmogenic effects of divided doses of intracoronary norepinephrine (50-200 ng.kg-1.min-1) in the absence and the presence of adenosine deaminase (5 U.kg-1.min-1). A dose of norepinephrine (100 ng.kg-1.min-1) that caused 66 +/- 17% ectopy in the absence of adenosine deaminase caused only 16 +/- 14% ectopy (P less than 0.05) in the presence of the enzyme. Ventricular tachycardia caused by 200 ng.kg-1.min-1 norepinephrine was reduced from 1.2 +/- 0.3 to 0.1 +/- 0.1 bouts/10 cardiac cycles (P less than 0.05) by adenosine deaminase. In five additional dogs, intracoronary adenosine (0.11 mumol/min) terminated sustained norepinephrine-induced (200 ng.kg-1.min-1) ventricular tachycardia within 23 +/- 9 s (P less than 0.05). As long as the adenosine infusion was maintained, a normal sinus rhythm was observed. We conclude that both adenosine and adenosine deaminase significantly attenuate norepinephrine-induced ventricular arrhythmias. A common element beyond the deamination of adenosine, quite possibly ammonia, appears to account for these results.