Central neural respiratory response to carotid sinus nerve stimulation in newborns

During exposure to hypoxia newborns hypoventilate following a brief period of hyperventilation. Failure of integration of the afferent signals from peripheral O2 chemoreceptors due to immaturity of the central respiratory centers could explain this paradoxical respiratory response. To test this hypothesis we have utilized anesthetized, paralyzed, mechanically ventilated newborn piglets and lambs (less than 11 days) and old piglets (19-35 days). The vagus nerves were cut in each animal. Respiratory activity was quantified by integration of phrenic neural activity. A carotid sinus nerve (CSN) was isolated and electrically stimulated for periods of 1-6 min. In all three groups of animals respiratory activity was continuously elevated throughout the period of CSN stimulation. After CSN stimulation respiratory activity immediately declined about 25% from the stimulated value. Thereafter respiratory activity declined in an exponential fashion toward the initial control level of respiratory activity. The time constant of this latter decay was 84.2 s in the young piglets, 83.2 s in the old piglets, and 63.0 s in the lambs. These results indicate that the respiratory centers of newborn piglets and lambs can maintain integration of continuous afferent CSN activity. Further, the respiratory afterdischarge that follows CSN stimulus cessation is similar to that of adults. These studies indicate that, during periods of O2 sufficiency, the central respiratory centers of newborns respond in a qualitatively similar manner to CSN stimulation as do adult cats.