Nitrous oxide and the baroreceptor reflexes in the dog

Abstract

The effects were studied of 67% nitrous oxide on the baroreceptor control of systemic haemodynamics in the dog. Nitrous oxide was added to end-tidal halothane concentrations of about 0.9% (H2) together with halothane levels approximately 25% above (H3) and below (H1) the H2 concentration. Baroreceptor function was assessed by brachiocephalic artery occlusion (BCO) or perfusion of the isolated carotid sinuses. In the intact animal, nitrous oxide significantly increased mean arterial pressure only at the H2 level (P less than 0.001). At the closed loop operating point of the carotid sinus reflex (CSR), for all halothane levels, nitrous oxide decreased cardiac output and stroke volume, increased systemic vascular resistance and central venous pressure with no effect upon mean arterial pressure. The operating point gain of the CSR was significantly depressed by nitrous oxide at the H1 and H3 levels (P less than 0.05). The CRS operating characteristics were significantly modified by N2O in a manner which depended upon the underlying concentration of halothane.