Prolonged apnea in infant monkeys resulting from stimulation of superior laryngeal nerve.
We measured characteristics of apnea resulting from electrical stimulation of the superior laryngeal nerve (SLN) in 28 anesthetized infant monkeys ranging from a gestational age of 141 days to 49 days postterm and in four adult monkeys. Progressive reduction in ventilation accompanied weak suprathreshold SLN stimulation. Poststimulus apnea followed stronger stimulation. Apnea duration was directly proportional to stimulus duration, provided that stimulus intensity was at least 1.5 X threshold. Poststimulus apnea periods were briefer in older infants and did not occur in adults. Pao2 measurements in four animals showed that lower values were associated with the longer poststimulus apnea episodes. Upper airway resistance measurements obtained from a subglottal cannula revealed that glottal closure was transiently associated with the onset of SLN stimulation, but the degree of closure diminished during the course of stimulation and was not present during the subsequent period of apnea. The parameters of SLN stimulation determine specific changes in cardiovascular functions independently of their respiratory effects. The results suggest that a brief afferent input from the SLN may have prolonged effects on respiratory regulation in infants. These persisting effects may be an important consideration in sudden infant death syndrome mechanisms.
D000403:Airway Resistance; D000818:Animals; D000831:Animals, Newborn; D001049:Apnea / Q000209:etiology*; D001794:Blood Pressure; D004195:Disease Models, Animal; D004558:Electric Stimulation; D005865:Gestational Age; D005931:Glottis / Q000503:physiopathology; D000882:Haplorhini; D006339:Heart Rate; D007823:Laryngeal Nerves / Q000502:physiology; D008251:Macaca; D008253:Macaca mulatta; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D013398:Sudden Infant Death
D010100:Oxygen