Site of Hypersensitiveness of the Exaggerated Sinus Caroticus Reflex

Abstract

Before Hering's 1 discovery of the carotid sinus reflex, the slowing of the pulse which results from pressure over the upper area of the carotid artery, particularly on the right side of the neck, was interpreted as the direct effect of pressure upon the vagus nerve. Variations in the effect on heart rhythm were considered as indicative of the condition of the heart muscle and the Wenckebach 2 school particularly attempted to use such differences in the prognostication of heart disease. Weil:1 agreed with Wenckebach that a prolonged cardiac arrest was due to a hypersensitiveness of the vagus endings in the myocardium consequent on pathological changes in the heart. Hering, having discovered that a reflex mechanism and not a direct stimulation is at play, became interested in the receptor organs of the afferent branch of the arc rather than in the end organs of the different efferent branches. He considered that a marked slowing of the pulse on pressure over the sinus caroticus was due to a hypersensitiveness of the afferent nerve endings induced by arterial sclerosis in this region. Consequently, Hering and his collaborators are inclined to use these same variations in heart rhythm after pressure over the carotid sinus as indicative of arterial sclerosis of the carotid artery. The experiments here reported were undertaken to determine whether the hypersensitivity in the exaggerated cardio-inhibitory response is in the afferent or efferent branches of the arc. The demonstration by Hering 1 that pressure on the sinus caroticus elicits 2 independent effects, (1) cardio-inhibitory effect, (2) vasodepressor effect, permitted the following approach to the problem. The afferent pathway for both reflexes is a common one by way of the sinus nerve through the glossophalangeal nerve to the central nervous system.