DOSE-DEPENDENT EFFECTS OF HALOTHANE ON TBE CARBON-DIOXIDE RESPONSES OF EXPIRATORY AND INSPIRATORY BULBOSPINAL NEURONS AND THE PHRENIC-NERVEACTIVITIES IN DOGS

Background: Expiratory bulbospinal and inspiratory bulbospinal neurons in the ventral respiratory group provide drive for thoracoabdominal e xpiratory and phrenic and thoracic inspiratory motor neurons. Potent i nhalational agents such as halothane may have differential effects on inspiratory and expiratory neurons, but detailed studies comparing neu rons at a homologous level are lacking. Methods: The dose-dependent ef fects of anesthesia with 1.0-2.5 minimum alveolar concentration haloth ane on the CO2 responses of single expiratory and inspiratory bulbospi nal neurons of the ventral respiratory group and on phrenic neural act ivities were studied in nonpremedicated, anesthetized, paralyzed, vago tomized dogs. Hyperventilation with O-2 and the addition of CO2-O-2 mi xtures were used to produce low, medium, and high steady-state levels of central CO2 drive. Results: Peak neuron discharge frequency decreas ed progressively with increasing halothane dose at all levels of CO2 d rive for both types of neurons. The sensitivities of inspiratory and e xpiratory bulbospinal neuronal activities to halothane were not signif icantly different from one another, whereas the sensitivity to halotha ne of the peak phrenic activity was markedly greater than those of the neurons. Increasing halothane dose caused a downward, predominantly p arallel shift of the CO2 response curves. Phrenic nerve activity also showed a decrease in slope of the CO2 response. Conclusions: The activ ities of respiratory premotor neurons are less depressed by increasing doses of halothane than is phrenic nerve activity. The greater depres sion of phrenic activity may result from additional anesthetic actions on the efferent motor pathways, resulting in decreased descending syn aptic inputs to phrenic motor neurons.