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Hypoxia reinforces laryngeal reflex bradycardia in infants.

Artikel i vetenskaplig tidskrift
Författare Göran Wennergren
T Hertzberg
J Milerad
Jan Bjure
H Lagercrantz
Publicerad i Acta paediatrica Scandinavica
Volym 78
Nummer/häfte 1
Sidor 11-7
ISSN 0001-656X
Publiceringsår 1989
Publicerad vid Institutionen för pediatrik
Sidor 11-7
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Blood Gas Monitoring, Transcutaneous, Chemoreceptor Cells, physiology, Heart Rate, Humans, Hypoxia, physiopathology, Infant, Infant, Newborn, physiology, Laryngeal Nerves, physiology, physiopathology, Larynx, physiology, physiopathology, Reflex, physiology, Respiration, Risk Factors, Sudden Infant Death, physiopathology
Ämneskategorier Fysiologi, Pediatrik

Sammanfattning

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 PO2 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 PO2-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.

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