BARORECEPTOR CONTROL OF SYSTEMIC HEMODYNAMICS AT INCREMENTAL HALOTHANE LEVELS IN THE DOG

The open-loop carotid sinus reflex control of systemic hemodynamics was studied in an acute dog preparation with isolated perfused carotid sinuses at 3 end-tidal halothane levels of 0.66 .+-. 0.02% (H1); 0.88 .+-. 0.02% (H2); and 1.17 .+-. 0.02% (H3), to investigate the dose dependency of the carotid sinus reflex operating characteristics for halothane. Corresponding to the above halothane levels were reflex operating point pressures (set point pressures) of 104.9 .+-. 2.9, 103.3 .+-. 4.1 and 76.0 .+-. 3.8 mmHg, respectively. Carotid sinus reflex gain decreased significantly with progressively increasing halothane levels (1.41 .+-. 0.18; 0.84 .+-. 0.12; 0.48 .+-. 0.09), as did the range of reflex changes in systemic arterial pressure for equal overall changes in carotid sinus pressure (87.1 .+-. 7.9; 64.1 .+-. 7.4; 33.6 .+-. 5.1 mmHg; P < 0.01). For halothane levels below .apprx. 0.9%, this depression was not dependent upon changes in mean systemic arterial pressure. The relationship between reflex gain and halothane concentration could be described by a 1st-order exponential which suggested virtual ablation of the carotid sinus reflex control of mean arterial pressure at an end-tidal halothane concentration exceeding about 1.6%.