Interaction of excitatory and inhibitory respiratory afterdischarge mechanisms in piglets.

Afferent inputs to the central neuronal networks responsible for respiratory control can have effects on respiratory output that persist even after cessation of the original stimulus. In adults, carotid sinus nerve (CSN) stimulation activates a central excitatory mechanism which causes prolonged elevation of respiratory output. In newborns, superior laryngeal nerve (SLN) stimulation activates a central inhibitory mechanism which causes prolonged inhibition of respiratory output. The present study was designed to confirm that CSN stimulation in newborns also activates a long-acting central excitatory mechanism and to determine in what way the long-acting excitatory and inhibitory mechanisms interact. Anesthetized, paralyzed, and vagotomized piglets (2-30 days) were studied. Integrated phrenic nerve activity was determined before, during, and after stimulus trials consisting of CSN and SLN stimulation alone or following trials of sequential or simultaneous CSN and SLN stimulation. Respiratory output following CSN stimulation remained elevated and only gradually declined to the base-line value. Respiratory output following SLN stimulation remained depressed and only gradually recovered to the base-line value. One minute after cessation of the sequential trials, the respiratory output was intermediate between that of CSN or SLN stimulation alone at equivalent poststimulus times. We conclude that the central neural mechanisms which mediate the persistent poststimulus effects of CSN and SLN stimulation are independent but that they interact for a prolonged period following simultaneous or sequential activation. In infants, this interaction may effect respiratory stability during episodes of central or obstructive apnea and hypoxia.