The therapeutic versatility of atropine is a longestablished pharmacologic concept. The ability of this drug to produce inhibition of vagal action on the heart is responsible for its traditional role in the treatment and prevention of bradycardia and cardiac arrhythmias. Although the intravenous administration of 2 mg has been considered adequate to produce complete blockade of vagal action on the sino-atrial node in man, there has been little documented evidence to confirm the dose range necessary to achieve maximal effect on heart rate. Dual control of heart rate by both parasympathetic and sympathetic systems has made it difficult for investigators to study the effects of atropine under conditions of nonsurgical isolation of the heart from sympathetic influences. The recent availability of β-sympathetic antagonists has made possible pharmacologic blockade, thus permitting a more accurate estimation of the alterations in vagal tone effected by atropine.
Chamberlain and associates1 have recently reported