Influence of beta-adrenergic and vagal activity on the effect of exogenous adenosine on supraventricular tachycardia termination

Adenosine, which binds to cell surface receptors and couples with guanosine triphosphate-binding inhibitory proteins (G(i)), is potent in terminating supraventricular tachycardia (SVT). However, whether the differences in autonomic tone will influence this effect remains unknown. This study was designed to investigate the role of β-adrenergic and vagal activity on the action of adenosine. Forty patients with clinically documented SVT (22 with atrioventricular node reentrant tachycardia and 18 with atrioventricular reciprocating tachycardia) were divided into 4 groups with 10 patients in each group. In groups 1 and 2, adenosine was intravenously injected during the baseline state and during infusion of isoproterenol (2 and 4 μg/min, respectively). Group 2 patients received atropine (0.04 mg/kg) injection before isoproterenol infusion. In groups 3 and 4, intravenous injection of adenosine was given during the baseline state and after injection of atropine (0.02 and 0.04 mg/kg, respectively). Group 4 patients received propranolol (0.2 mg/kg) before atropine injection. The minimal dose of adenosine to terminate tachycardia during isoproterenol infusion of 2 μg/min was greater than that during the baseline state in both groups 1 and 2. The minimal dose of adenosine during isoproterenol infusion with 4 μg/min was higher than that with 2 μg/min in group 2, but not in group 1 patients. In both groups 3 and 4, the minimal dose of adenosine required to terminate tachycardia during atropine injection with 0.02 mg/kg was greater than that during the baseline state. The minimal effective dose of adenosine during atropine injection with 0.04 mg/kg was higher than that with 0.02 mg/kg in group 4, but not in group 3 patients. In conclusion, either limb of the autonomic nervous system may modulate the adenosine dosage required for termination of SVT. Patients taking drugs such os β blockers or vagolytic agents may need alterations in the dose of adenosine for therapy.