ROLE OF SUBSTANCE-P IN THE LARYNGEAL CHEMOREFLEX

The laryngeal chemoreflex (LCR) is a potentially life-threatening refl ex that is elicited in immature animals by the topical application of water to the laryngeal mucosa. The reflex response is characterized by immediate apnea and laryngeal adduction and delayed cardiovascular in stability. The cardiorespiratory changes of the LCR may be life-threat ening, particularly in very immature animals such as piglets under 2 w eeks of age. The afferent and efferent limbs of the LCR are mediated t hrough the vagus nerve, but the neuromediators responsible for the ref lex changes have not yet been clearly elucidated. Previous agonist and antagonist studies in immature dogs demonstrated that substance P, a sensory tachykinin, mediates the life-threatening esophagolaryngeal ad ductor reflex elicited by distal esophageal sensory nerve stimulation. This study was conducted to determine if substance P also plays a rol e in mediating the LCR. The LCR response was compared before and after treatment with intravenous substance P antagonist (Pfizer CP-96,345-1 ) in eight piglets (mean 27.7 days of age). The laryngeal and cardiova scular responses of the animals following intravenous administration o f the tachykinins substance P, neurokinin A, and neurokinin B were als o assessed. Pretreatment with substance P antagonist did not alter the LCR's duration of apnea (p > .10), laryngeal adductor response, or ea rly change in mean arterial pressure (p >.10), although the early maxi mal heart rate response was significantly altered (p < .01). Intraveno us substance P, neurokinin A, and neurokinin B did not reproduce the l aryngeal respiratory response of the LCR. We conclude that substance P , neurokinin A, and neurokinin B are not key neurotransmitters of the LCR.