A Mechanism of Reflexogenic Bradycardia produced by Cardiac Glycosides

Abstract

IT has been accepted that the vagal factor is one of the most important factors concerning the production of bradycardia by cardiac glycosides^1,2. However, the bradycardia produced by cardiac glycosides was not prevented completely by bilateral vagotomy or previous administration of atropine³. Gold et al.⁴ called the latter factor the extravagal factor, which was considered to be a direct action of cardiac glycosides on the heart. On the other hand, cardiac glycosides did not exert a definite negative chronotropic action on the isolated mammalian heart^5,6. In order to elucidate this discrepancy, the following experiments were carried out on cats using strospeside as the cardiac glycoside.