Abstract
Arterial baroreceptor function was assessed in trained, chronically instrumented dogs by measuring the systemic hemodynamic responses to brachiocephalic artery occlusion (BCO). BCO was carried out in awake dogs and repeated at end-tidal halothane levels of 0.75 .+-. 0.01% (H1), 0.94 .+-. 0.02% (H2) and 1.13 .+-. 0.02% (H3). Before BCO, at H1 only the increased heart rate and decreased stroke volume were significantly different from awake controls (P < 0.01). Mean arterial pressure and cardiac output at H2 and H3 were significantly lower than in the awake controls (P < 0.05). The pressor response to BCO fell progressively with increasing halothane levels, the decrease being significant at the H2 and H3 levels (P < 0.001). There was a good linear correlation between the pressor response to BCO as a percentage of the response in awake animals, and the end-tidal halothane levels, (r = -0.816, P < 0.001).This indicated a sensitive dose-dependent modification of the hemodynamic response to BCO by halothane. Halothane levels existed between .apprx. 0.7-0.8%, at which levels the average pressor response to BCO was not significantly different from awake values.