Document Detail


Inhibitory effects of hyperthermia on mechanisms involved in autoresuscitation from hypoxic apnea in mice: a model for thermal stress causing SIDS.
MedLine Citation:
PMID:  15247199     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The physiological mechanisms that might be involved in an association between heat stress and sudden infant death syndrome (SIDS) are obscure. We tested the hypothesis that a combination of acute hypoxia and elevated body temperature (T(B)) might prevent autoresuscitation from hypoxic apnea (AR). We exposed 21-day-old mice (total = 216) to hyperthermia (40.5-43.5 degrees C), hypoxia, or a combination of the two. Neither hyperthermia alone (40.5-42.5 degrees C) nor hypoxia alone was found to be lethal, but the combination produced failure to AR during the first hypoxic exposure with increasing frequency as T(B) increased. The ability to withstand multiple hypoxic exposures was also reduced as T(B) increased. In contrast, heat stress causing moderate T(B) increase (40.5 degrees C) had no effect on survival. Increased T(B) (43.5 degrees C) reduced gasping duration and number of gasps. It increased heart rate during anoxia but did not alter gasping rate. Furthermore, the oxygen-independent increase in heart rate observed before gasping failure was usually delayed until after the last gasp in hyperthermic animals. Mild dehydration occurred during T(B) elevation, but this did not appear to be a primary factor in AR failure. We conclude that a thermal stress, which by itself is nonlethal, frequently prevents AR from hypoxic apnea. This may be due, at least in part, to decreased gasp number and duration as well as to hyperthermia-related asynchrony of reflexes regulating heart and gasping frequencies during attempted AR.
Authors:
Levent Kahraman; Bradley T Thach
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  97     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2004 Aug 
Date Detail:
Created Date:  2004-07-12     Completed Date:  2005-01-14     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  669-74     Citation Subset:  IM    
Affiliation:
Edward Mallinckrodt Department of Pediatrics, Washington University School of Medicine, 660 S. Euclid, Campus Box 8208, St. Louis, MO 63110, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / complications,  mortality,  physiopathology*
Apnea / complications,  mortality,  physiopathology*
Body Temperature
Body Weight
Colon
Dehydration / complications,  mortality,  physiopathology
Female
Fever / complications,  mortality,  physiopathology*
Heart Rate
Humans
Infant
Male
Mice
Mice, Inbred C57BL
Respiratory Mechanics
Resuscitation
Sudden Infant Death / etiology*
Grant Support
ID/Acronym/Agency:
HD-10993/HD/NICHD NIH HHS

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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