Abstract

We tested the hypotheses that elevated body temperature would prolong reflex apnea following electrical stimulation of the superior laryngeal nerve (SLN) in decerebrate neonatal piglets and that thermal prolongation of reflex apnea after stimulation of the SLN depended on GABAergic mechanisms. These studies were conducted in 13 decerebrate piglets (age 3-15 days). The SLN was stimulated at approximately 1.5 times the threshold stimulus level for 10 s starting at the beginning of inspiration. We measured the duration of the apnea and respiratory disruption that followed SLN stimulation. Elevating body temperature prolonged the duration of the apnea and respiratory disruption that followed SLN stimulation, and treatment with antagonists of gama-aminobutyric acid A-type (GABAA) receptors reversed the thermal prolongation of reflex apnea and the period of respiratory disruption even though body temperature remained elevated. We conclude that elevated body temperature enhances or amplifies GABAergic mechanisms that prolong the respiratory inhibition following electrical stimulation of the SLN.

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