抄録
In spite of numerous reports on bradycardia produced by cardiac glycosides hitherto, the mechanism is not completely clarified.
Ackermann (1) reported that early digitalis bradycardia was prevented by vagal severance or by administration of atropine. This observation has generally been accepted. Heymans and Heymans (2) obtained additional evidence using cross-circulation dogs. They reported that ouabain-induced bradycardia was not due to the central action of ouabain but had its origin in the vagal reflex. Furthermore, Hering (3) and Heymans et al. (4, 5) showed that ouabain-induced bradycardia was nullified by severing both sinus nerves and both cardio-aortic nerves in dogs. Morimoto et al. (6) also demonstrated that digitalis bradycardia was prevented by destruction of the carotid sinus tissues and resection of cardio-aortic nerves in dogs. Fukuda and his associates (7, 8) maintained that the bradycardia produced by large doses of digitalis was mainly due to the cardio-cardiac reflex. This assertion is supported by the fact that the action potentials of cardiac nerves (centripetal vagal nerves) increased by cardiac glycoside administration in cats (9). However, Schmitt et al. (10, 11) found that the action potentials originating in the chemoreceptors in the carotid body were increased by cardiac glycosides and they concluded that the chemoreceptors were closely related to the occurrence of digitalis bradycardia in cats.
Thus, opinions have differed on the origin and pathways of impulses of reflexogenic bradycardia produced by cardiac glycosides.
The present study was conducted to elucidate the probable pathways of the reflex by which cardiac glycosides produce bradycardia.
