Halothane effects on ventilatory responses to changes in intrapulmonary CO2 in geese.

Experiments were conducted to test the hypothesis that halothane anesthesia functionally disrupts CO2-sensitive intrapulmonary chemoreceptors (IPC) in birds. Halothane effects on ventilatory reflexes elicited by changes in lung CO2 without extrapulmonary halothane or CO2 effects were studied in 6 anesthetized (pentobarbital, 30 mg/kg) and unidirectionally ventilated geese. Each lung was independently ventilated. Halothane was added only to gases ventilating the left lung. The left pulmonary artery was occluded to prevent changes in PCO2 or halothane concentration within the left lung from affecting arterial blood. The right lung allowed control of arterial blood gases and was vagally denervated. Left lung CO2 reflexes were observed at different levels of halothane concentration between 0 and 2% while arterial PCO2 and PO2 were held constant. Higher levels of chemical drive were necessary to initiate ventilatory movements in geese (PACO2 = 40-60 mmHg) relative to previous reports on chickens using similar experimental procedures (PaCO2 less than or equal to 30 mmHg). The amplitude of sternal movements or respiratory amplitude (RA) increased as left lung PCO2 increased from 6 to 55 mmHg, and then reached a plateau. Adding halothane (1 or 2%) to the left lung increased RA through a limited range of PCO2, but had no effect on its maximum value. Neither CO2 nor halothane in the left lung had any effect on respiratory frequency. We conclude that halothane impairs lung CO2 reflexes largely due to its effects on IPC since intrapulmonary halothane augments ventilatory activity at low, but not high intrapulmonary PCO2. Effects of halothane on IPC may play a role in the unique ventilatory effects of halothane anesthesia in intact, spontaneously breathing birds relative to mammals at equipotent anesthetic levels.