BLOCKADE WITH DICHLOROISOPROTERENOL (DCI) OF THE SYMPATHETIC FACTOR OF STROSPESIDE INDUCED BRADYCARDIA IN CATS

Abstract

While it has clearly been demonstrated by Heymans and Heymans (1, 2) that vagovagal reflex participates in the production of bradycardia by cardiac glycosides, other investigators have reported that cardiac glycosides were capable of producing bradycardia even after administration of atropine (3) or severance of both vagus nerves (4, 5). Thus, these evidences seem to be contradictory to the results obtained by Heymans and Heymans (1, 2). On the other hand in 1939, Gold and his associates (6, 7) pointed out that two factors (vagal and extravagal) participated in the production of bradycardia by cardiac glycosides. This suggestion is convenient for the interpretation of the contradictory evidences stated above. On the extravagal factor of bradycardia, however, reports are conflicting and no complete opinion has been established.
In a previous paper, Abiko (5) suggested hypothetically that the reflex route composed of the carotid sinus nerve, medulla, cervical cord, stellate ganglion, and the sympathetic fibers to the heart was an extravagal factor of bradycardia produced by cardiac glycosides. And, the hypothetical reflex pathway was supported partially by the evidence (8) that bradycardia produced by strospeside was in accord with inhibition of the efferent discharges in the pre and post-ganglionic stellate fibers in vagotomized cats.
The present study was also designed to test the possibility of the sympathetic portion of the hypothetical reflex pathway as one of the extravagal factors of bradycardia produced by cardiac glycosides. The present experiments were conducted on the basis of the following expectation: “If the extravagal mechanism of bradycardia by cardiac glycosides is really concerned with sympathetic cardiac nerves, bradycardia by cardiac glycosides may be prevented by blocking the neuro-muscular transmission at the site of adrenergic receptor of the heart in vagotomized animals.” For this purpose, dichloroisoproterenol (DCI) (9-12) was used as the beta-type adrenergic blocking agent in this experiments. Strospeside was used as a cardiac glycoside because of its high potency to produce bradycardia.