Abstract
It has generally been accepted that the vagal effect participates in bradycardia due to cardiac glycosides (1, 2). However, the vagal effect may not be the only factor which produces the cardiac slowing, because cardiac glycosides can produce bradycardia even after bilateral severance of vagus nerves or under the effect of atropine (3, 4). Gold et al. (5, 6) suggested a direct bradycardiac action of cardiac glycosides on the heart muscle. However, the results on the effect of cardiac glycosides on the heart rate are still controversial in the experiments with isolated hearts. Heymans et al. (7, 8) reported that cardiac glycosides did not produce bradycardia in dogs when vagus nerves and also carotid sinus nerves were completely severed. The present author has also obtained a similar finding in cats using a cardiac glycoside, strospeside (9).
In recent work of the present author (9), a hypothesis has been postulated on the mechanism of bradycardia produced by cardiac glycosides: There are two different kinds of nervous reflex systems, quite independent of each other, in producing bradycardia by cardiac glycosides. One is the vago-vagal reflex and the other is the carotid body-sympathetic nervous reflex chain possibly composed of the sinus nerve, cervical cord, stellate ganglion and the sympathetic fibers to the heart.
The purpose of the present experiment is the presentation of some evidences for the possibility of the sympathetic portion of the hypothetical carotid body-sympathetic nervous chain, which is assumed to be the extravagal factor, by observing the effect of strospeside on the efferent discharges in the cardiac sympathetic nerves in cats.
