Elevated body temperature enhances the laryngeal chemoreflex in decerebrate piglets

Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire Submitted 20 August 2004 ; accepted in final form 10 November 2004 Hyperthermia and reflex apnea may both contribute to sudden infant death syndrome (SIDS). Therefore, we investigated the effect of increased body temperature...

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Veröffentlicht in:Journal of applied physiology (1985) 2005-03, Vol.98 (3), p.780-786
Hauptverfasser: Curran, A. K, Xia, L, Leiter, J. C, Bartlett, D., Jr
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Sprache:eng
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Zusammenfassung:Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire Submitted 20 August 2004 ; accepted in final form 10 November 2004 Hyperthermia and reflex apnea may both contribute to sudden infant death syndrome (SIDS). Therefore, we investigated the effect of increased body temperature on the inhibition of breathing produced by water injected into the larynx, which elicits the laryngeal chemoreflex (LCR). We studied decerebrated, vagotomized, neonatal piglets aged 3–15 days. Blood pressure, end-tidal CO 2 , body temperature, and phrenic nerve activity were recorded. To elicit the LCR, we infused 0.1 ml of distilled water through a polyethylene tube passed through the nose and positioned just rostral to the larynx. Three to five LCR trials were performed with the piglet at normal body temperature. The animal's core body temperature was raised by 2.5°C, and three to five LCR trials were performed before the animal was cooled, and three to five LCR trials were repeated. The respiratory inhibition associated with the LCR was substantially prolonged when body temperature was elevated. Thus elevated body temperature may contribute to the pathogenesis of SIDS by increasing the inhibitory effects of the LCR. neonatal piglets; hyperthermia Address for reprint requests and other correspondence: J. C. Leiter, Dept. of Physiology, Dartmouth Medical School, Lebanon, NH 03756 (E-mail: james.c.leiter{at}dartmouth.edu )
ISSN:8750-7587
1522-1601
DOI:10.1152/japplphysiol.00906.2004