Carotid chemoreceptor stimulation and ventricular performance

Abstract

In paced, canine, innervated, isovolumetric, left ventricle preparations in which the lungs were deflated, hypoxia of the isolated carotid sinus region usually elicited a negative inotropic effect on left ventricular performance, as assessed by peak pressure development. After vagotomy, a slight increase in peak left ventricular pressure was usually evoked. It is concluded that the primary reflex cardiac effect of carotid chemoreceptor stimulation consists of an increase in vagal tone. When the vagi are intact this augmentation of parasympathetic activity is primarily responsible for the depression of ventricular performance, and for bradycardia in the unpaced heart. After vagotomy, carotid chemoreceptor stimulation produces a slight increase in sympathetic activity under the conditions of the present study. This effect may actually be secondary to excitation of the respiratory centers, which results from chemoreceptor stimulation.