Extent and mechanism of halothane sensitization of the carotid sinus baroreceptors.

The present study was performed to determine the extent and mechanism of carotid sinus baroreceptor sensitization due to halothane in an isolated, denervated carotid sinus in anesthetized dogs (thiopental 25 mg/kg; 5 mg X kg-1 X h-1, maintenance dose). Efferent sympathetic nerves to the sinus were sectioned to eliminate the contribution of these fibers to any sensitization observed. Halothane (H) administration was localized to the carotid sinus by an isolated perfusion system. The perfusion system was used to make standardized sine wave changes in carotid sinus pressure. Carotid sinus afferent nerve activity from single or few-fiber nerve preparations was recorded during carotid sinus pressure changes and the slopes of nerve activity versus carotid sinus pressure were used to determine the gain, or sensitivity, of the baroreceptors. The addition of 0.75% H and 1.5% H to the sinus perfusion produced a dose-dependent sensitization of the baroreceptors. A greater increase in carotid sinus afferent nerve activity for a given increase in sinus pressure was used as an indication of an increase in receptor sensitivity, or sensitization. In the presence of sodium nitroprusside, given in doses to maximally dilate the sinus prior to H administration, only 1.5% H produced baroreceptor sensitization. This suggests the changes in sinus wall tension due to halothane may have contributed to the sensitization seen during H administration. The remaining sensitization at 1.5% H was eliminated in the presence of nitroprusside and 7.5 mM Ca++. This remaining sensitization therefore appears to be Ca++-related and may be due to direct effects of H on the baroreceptors.