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Acetylcholine released from cholinergic nerves contributes to cutaneous vasodilation during heat stressNitric oxide (NO) contributes to active cutaneous vasodilation during a heat stress in humans. Given that acetylcholine is released from cholinergic nerves during whole body heating, coupled with evidence that acetylcholine causes vasodilation via NO mechanisms, it is possible that release of acetylcholine in the dermal space contributes to cutaneous vasodilation during a heat stress. To test this hypothesis, in seven subjects skin blood flow (SkBF) and sweat rate were simultaneously monitored over three microdialysis membranes placed in the dermal space of dorsal forearm skin. One membrane was perfused with the acetylcholinesterase inhibitor neostigmine (10 microM), the second membrane was perfused with the NO synthase inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME; 10 mM) dissolved in the aforementioned neostigmine solution (l-NAME(Neo)), and the third membrane was perfused with Ringer solution as a control site. Each subject was exposed to approximately 20 min of whole body heating via a water-perfused suit, which increased mean body temperature from 36.4 +/- 0.1 to 37.5 +/- 0.1 degrees C (P < 0.05). After the heat stress, SkBF at each site was normalized to its maximum value, identified by administration of 28 mM sodium nitroprusside. Mean body temperature threshold for cutaneous vasodilation was significantly lower at the neostigmine-treated site relative to the other sites (neostigmine: 36.6 +/- 0.1 degrees C, l-NAME(Neo): 37.1 +/- 0.1 degrees C, control: 36.9 +/- 0.1 degrees C), whereas no significant threshold difference was observed between the l-NAME(Neo)-treated and control sites. At the end of the heat stress, SkBF was not different between the neostigmine-treated and control sites, whereas SkBF at the l-NAME(Neo)-treated site was significantly lower than the other sites. These results suggest that acetylcholine released from cholinergic nerves is capable of modulating cutaneous vasodilation via NO synthase mechanisms early in the heat stress but not after substantial cutaneous vasodilation.
Document ID
20040088025
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Shibasaki, Manabu
(Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas Texas 75231, United States)
Wilson, Thad E.
Cui, Jian
Crandall, Craig G.
Date Acquired
August 21, 2013
Publication Date
December 1, 2002
Publication Information
Publication: Journal of applied physiology (Bethesda, Md. : 1985)
Volume: 93
Issue: 6
ISSN: 8750-7587
Subject Category
Life Sciences (General)
Funding Number(s)
CONTRACT_GRANT: HL-67422
CONTRACT_GRANT: HL-10488
CONTRACT_GRANT: HL-61388
Distribution Limits
Public
Copyright
Other
Keywords
Non-NASA Center
Clinical Trial
NASA Discipline Cardiopulmonary

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