Baroreceptor reflexes and pulmonary hemodynamics during halothane and halothane-nitrous oxide anesthesia in the dog.

The effects of reflexly induced changes in sympathetic nerve activity on pulmonary hemodynamics during halothane and halothane-nitrous oxide anesthesia were investigated. Perfusion pressure was changed in the isolated carotid sinuses (60 to 180 mm Hg) of vagotomized, open-chested dogs, anesthesized at three end-tidal halothane concentrations of 0.66% +/- 0.02% (H1), 0.88% +/- 0.02% (H2), and 1.16% +/- 0.03% (H3) with and without 67% nitrous oxide. At no levels of carotid sinus pressure were pulmonary vascular resistance or pulmonary input resistance affected by halothane or nitrous oxide. With increasing carotid sinus stimulation, pulmonary vascular resistance increased at high levels of carotid sinus pressure at the H3 halothane level and with nitrous oxide at the H1 level. Changes in pulmonary input resistance were opposite in direction to baroreceptor stimulation and were greatest at the H3 level with nitrous oxide. Thus for a wide range of baroreceptor stimulation, pulmonary vascular resistance and pulmonary input resistance remained constant at end-tidal halothane concentrations of approximately 0.9%, with or without nitrous oxide. Only when halothane concentrations were significantly above or below 0.9% did reflex changes become significant, particularly with respect to the pulmonary component of the resistive load upon the right ventricle.