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Nitric oxide and cutaneous active vasodilation during heat stress in humans
1 Geriatric Research, Education, and Clinical Center, Department of Veterans Affairs, South Texas Veterans Health Care System, Audie L. Murphy Division, San Antonio 78284; Departments of 2 Physiology, 3 Medicine, and 4 Pharmacology, University of Texas Health Science Center at San Antonio, San A...
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Published in: | Journal of applied physiology (1985) 1998-09, Vol.85 (3), p.824-829 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 1 Geriatric Research,
Education, and Clinical Center, Department of Veterans
Affairs, South Texas Veterans Health Care System, Audie L. Murphy
Division, San Antonio 78284; Departments of
2 Physiology,
3 Medicine, and
4 Pharmacology, University of
Texas Health Science Center at San Antonio, San Antonio, 78284;
5 Institute for Exercise
and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas,
75231; and 6 University of
Texas Southwestern Medical Center, Dallas, Texas 75235
Whether nitric oxide (NO) is involved in
cutaneous active vasodilation during hyperthermia in humans is unclear.
We tested for a role of NO in this process during heat stress
(water-perfused suits) in seven healthy subjects. Two forearm sites
were instrumented with intradermal microdialysis probes. One site was
perfused with the NO synthase inhibitor
N G -nitro- L -arginine
methyl ester ( L -NAME)
dissolved in Ringer solution to abolish NO production. The other site
was perfused with Ringer solution only. At those sites, skin blood flow
(laser-Doppler flowmetry) and sweat rate were simultaneously and
continuously monitored. Cutaneous vascular conductance, calculated from
laser-Doppler flowmetry and mean arterial pressure, was normalized to
maximal levels as achieved by perfusion with the NO donor nitroprusside through the microdialysis probes. Under normothermic conditions, L -NAME did not significantly
reduce cutaneous vascular conductance. During hyperthermia, with skin
temperature held at 38-38.5°C, internal temperature rose from
36.66 ± 0.10 to 37.34 ± 0.06°C ( P |
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ISSN: | 8750-7587 1522-1601 |
DOI: | 10.1152/jappl.1998.85.3.824 |