In newborn animals, apnea induced by superior laryngeal nerve (SLN) electrical stimulation is a potentially lethal respiratory reflex. To study the recovery respiratory patterns following cessation of an apnea-producing stimulus, without confounding blood gas changes, 12 anesthetized gallamine-paralyzed piglets (<8 days age) were ventilated, and end-tidal CO2 was kept constant (mean PETCO2 32.9 ± 1.3 Torr). In addition, the vagus nerve of each piglet was sectioned bilaterally. Respiratory output was quantified by moving average of the rectified phrenic neurogram. Phrenic apnea was induced by stimulation of the central end of a SLN or cut vagus nerve for 2.5-45 s. SLN stimulation caused apnea that persisted for 1-48 s after stimulus cessation. The duration of poststimulus apnea was directly related to duration of SLN stimulation. Following a 10-s stimulus, respiratory output of the first recovery breath was reduced and required greater than 90 s to recover to control levels. Vagal stimulation also caused apnea but was not associated with either post stimulus apnea or prolonged respiratory inhibition. I conclude that SLN stimulation activates a central neural mechanism that inhibits respiratory output for a prolonged period after stimulus offset.
|Number of pages
|Journal of Applied Physiology Respiratory Environmental and Exercise Physiology
|Published - Jan 1 1981
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