Ventricular responses to hypoxemia following chemoreceptor denervation and adrenalectomy

Abstract

The sensory system responsible for increased ventricular contractility (VC) during hypoxemia is not fully established. Previous studies have demonstrated that isolated carotid body hypoxia is not associated with an increase of VC. 8 However, reflexly increased VC may result from pharmacologic stimulation of the aortic chemoreceptors. 9 In order to evaluate their contribution during hypoxia, VC was studied in atropinized cats before and following denervation by bilateral vagotomy. VC was measured under conditions of constant aortic pressure, cardiac output, and heart rate. Arterial blood gases and pH were continuously monitored. With hypoxemia (P o 2 27 to 46 mm. Hg), all cats showed an increase of VC, manifested by an increase of dP dt for a given end-diastolic pressure. The responses were unaltered by bilateral vagotomy. Similar findings were obtained in animals with bilateral carotid body denervation. The increase of VC during hypoxia was not significantly less following adrenalectomy. Beta-adrenergic blockade completely abolished these responses. It is concluded that the increase in VC associated with systemic hypoxia cannot be entirely attributed to aortic or carotid chemoreceptor reflex activity. The influence of stimulation of structures within the central nervous system must also be considered.