Pharmacologic study of respiratory afterdischarge

Abstract

Respiratory afterdischarge, an increased but slowly declining respiratory output lasting some minutes after cessation of a stimulus, is generated by a bulbopontine mechanism whose precise anatomic locus and neurophysiological mechanism are unknown. To determine if the mechanism responsible for the afterdischarge was due to one of the major long-acting central neurotransmitters, we studied a control group of animals and groups of animals that were pretreated with the antiserotonin agents, methysergide, parachlorophenylalanine, and 5,7-dihydroxytryptamine, the dopamine-norepinephrine antagonists alpha-methytyrosine and haloperidol, and the endorphin antagonist, naloxone. Anesthetized, paralyzed, vagotomized, and glomectomized cats were used. We measured phrenic activity before, during, and after carotid sinus nerve and calf muscle stimulation. None of the antagonists had an effect on the response to stimulation, on the magnitude of the afterdischarge, or on its time course during recovery. We conclude that these central neurotransmitters do not participate in the genesis of the respiratory afterdischarge.