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Hypoxia Reinforces Laryngeal Reflex Bradycardia in Infants
Author(s) -
WENNERGREN G.,
HERTZBERG T.,
MILERAD J.,
BJURE J.,
LAGERCRANTZ H.
Publication year - 1989
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.1989.tb10879.x
Subject(s) - medicine , bradycardia , reflex , apnea , sudden infant death syndrome , anesthesia , hypoxia (environmental) , cardiorespiratory fitness , peripheral chemoreceptors , heart rate , reflex bradycardia , cardiology , stimulation , pediatrics , blood pressure , carotid body , chemistry , organic chemistry , oxygen
. The laryngeal chemoreflex involves bradycardia, apnea, swallowing and peripheral vasoconstriction. This reflex was studied in twelve infants, aged 5 days‐28 weeks, who had sustained an apparent life‐threatening event or were siblings of infants who had died of the sudden infant death syndrome. The bradycardic and apneic components of the reflex were found to be significantly, and sometimes powerfully, reinforced when elicited by pharyngeal water instillation during acute, mild hypoxia (transcutaneous Po 2 4.6–8.3 kPa). Apnea duration during normoxia was 0.7–15 sec, and during hypoxia 2–30 sec. Heart rate change ranged from +26% to −21% during normoxia, as compared with −4% to −63% during hypoxia. The percentage change in heart rate was found to inversely correlate with the transcutaneous Po 2 ;‐level prevailing when the reflex was elicited. The conclusion is that there is a significant reinforcement of the cardiorespiratory adjustments when the laryngeal reflex is activated during simultaneous excitation of the peripheral arterial chemoreceptors. One infant, showing a particularly strong increase of the cardiorespiratory response to laryngeal receptor stimulation during hypoxia, later died of sudden infant death syndrome.