Document Detail


Human cardiorespiratory and cerebrovascular function during severe passive hyperthermia: effects of mild hypohydration.
MedLine Citation:
PMID:  18483173     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The influence of severe passive heat stress and hypohydration (Hypo) on cardiorespiratory and cerebrovascular function is not known. We hypothesized that 1) heating-induced hypocapnia and peripheral redistribution of cardiac output (Q) would compromise blood flow velocity in the middle cerebral artery (MCAv) and cerebral oxygenation; 2) Hypo would exacerbate the hyperthermic-induced hypocapnia, further decreasing MCAv; and 3) heating would reduce MCAv-CO2 reactivity, thereby altering ventilation. Ten men, resting supine in a water-perfused suit, underwent progressive hyperthermia [0.5 degrees C increments in core (esophageal) temperature (TC) to +2 degrees C] while euhydrated (Euh) or Hypo by 1.5% body mass (attained previous evening). Time-control (i.e., non-heat stressed) data were obtained on six of these subjects. Cerebral oxygenation (near-infrared spectroscopy), MCAv, end-tidal carbon dioxide (PetCO2) and arterial blood pressure, Q (flow model), and brachial and carotid blood flows (CCA) were measured continuously each 0.5 degrees C change in TC. At each level, hypercapnia was achieved through 3-min administrations of 5% CO2, and hypocapnia was achieved with controlled hyperventilation. At baseline in Hypo, heart rate, MCAv and CCA were elevated (P<0.05 vs. Euh). MCAv-CO2 reactivity was unchanged in both groups at all TC levels. Independent of hydration, hyperthermic-induced hyperventilation caused a severe drop in PetCO2 (-8+/-1 mmHg/ degrees C), which was related to lower MCAv (-15+/-3%/ degrees C; R2=0.98; P<0.001). Elevations in Q were related to increases in brachial blood flow (R2=0.65; P<0.01) and reductions in MCAv (R2=0.70; P<0.01), reflecting peripheral distribution of Q. Cerebral oxygenation was maintained, presumably via enhanced O2-extraction or regional differences in cerebral perfusion.
Authors:
Jui-Lin Fan; James D Cotter; Rebekah A I Lucas; Kate Thomas; Luke Wilson; Philip N Ainslie
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Publication Detail:
Type:  Journal Article     Date:  2008-05-15
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  105     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2008 Aug 
Date Detail:
Created Date:  2008-08-05     Completed Date:  2008-10-10     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  433-45     Citation Subset:  IM    
Affiliation:
Department of Physiology, Otago School of Medical Science, University of Otago, Dunedin, New Zealand.
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MeSH Terms
Descriptor/Qualifier:
Adult
Body Temperature / physiology
Carbon Dioxide / pharmacology
Cerebrovascular Circulation / physiology*
Dehydration / physiopathology*
Esophagus / physiology
Fever / physiopathology*
Humans
Hyperventilation / physiopathology
Hypocapnia / metabolism
Laser-Doppler Flowmetry
Male
Middle Cerebral Artery / physiopathology
Oxygen Consumption / physiology
Pulmonary Gas Exchange / physiology
Regional Blood Flow / physiology
Skin / blood supply
Supine Position / physiology
Chemical
Reg. No./Substance:
124-38-9/Carbon Dioxide
Comments/Corrections
Comment In:
J Appl Physiol. 2008 Aug;105(2):400-1   [PMID:  18535132 ]

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