Nitric oxide concentration increases in the cutaneous interstitial space during heat stress in humans

Abstract

. Nitric oxide concentration increases in the cutaneous interstitial space during heat stress in humans. J Appl Physiol 94: 1971Physiol 94: -1977Physiol 94: , 2003 10.1152/japplphysiol.00826. 2002To examine the role of nitric oxide (NO) in cutaneous active vasodilation, we measured the NO concentration from skin before and during whole body heat stress in nine healthy subjects. A forearm site was instrumented with a NO-selective, amperometric electrode and an adjacent intradermal microdialysis probe. Skin blood flow (SkBF) was monitored by laser-Doppler flowmetry (LDF). NO concentrations and LDF were measured in normothermia and heat stress. After heat stress, a solution of ACh was perfused through the microdialysis probe to pharmacologically generate NO and verify the electrode's function. During whole body warming, both SkBF and NO concentrations began to increase at the same internal temperature. Both SkBF and NO concentrations increased during heat stress (402 Ϯ 76% change from LDF baseline, P Ͻ 0.05; 22 Ϯ 5% change from NO baseline, P Ͻ 0.05). During a second baseline condition after heat stress, ACh perfusion led to increases in both SkBF and NO concentrations (496 Ϯ 119% change from LDF baseline, P Ͻ 0.05; 16 Ϯ 10% change from NO baseline, P Ͻ 0.05). We conclude that NO does increase in skin during heat stress in humans, attendant to active vasodilation. This result suggests that NO has a role beyond that of a permissive factor in the process; rather, NO may well be an effector of cutaneous vasodilation during heat stress. skin blood flow; vasodilation; amperometric electrode; thermoregulation THE HUMAN CUTANEOUS CIRCULATION is a major effector of thermoregulatory homeostasis. During periods of whole body heat stress, this circulation undergoes a profound reflex vasodilation to deliver blood, and hence heat, to the body's surface for removal to the environment. During periods of cold stress, the cutaneous blood vessels are intensely vasoconstricted to reduce loss of heat from the body to the environment. These reflex changes in skin blood flow (SkBF) occur in response to changes in internal temperature and skin temperature (T sk ) and are mediated by two branches of the sympathetic nervous system: an active vasodilator system and an active vasoconstrictor system (17).The mechanisms by which the active vasodilator system causes increases in SkBF during heat stress have been the subject of numerous investigations since the system was first described over 70 years ago (18). A number of these studies demonstrated that muscarinic-receptor blockade with atropine could slightly delay (10, 17, 19, 22) and attenuate (17, 19) the reflex increase in SkBF during heat stress. This finding of partial reductions in the active vasodilator response despite complete muscarinic-receptor blockade established a role for cholinergic nerves in the process of active vasodilation, but it left open to question the exact nature of this involvement. In 1995, our laboratory showed that thermoregulatory active vasodilation involve...

Does local heating-induced nitric oxide production attenuate vasoconstrictor responsiveness to lower body negative pressure in human skin?

“…Foremost is the possibility that endogenous concentrations of NO via local heating are likely different than concentrations achieved via exogenous administration of the NO donor sodium nitroprusside, despite similar magnitudes of increase in CVC between exogenous NO administration relative to local heating. This hypothesis would dictate that endogenous cutaneous NO concentrations achieved during local heating (3,10,16) are not sufficient to attenuate the effects of the cutaneous vasoconstrictor system.…”

Diminished skin vasodilator response to local heating in patients with long-standingsubacute myelo-optico-neuropathy

“…Therefore, involvement of sensory axon-reflex may attenuate SkBF rise at P2 as well as P1. In addition to CGRP and substance P, acetylcholine also has a vasodilator effect, which increases both SkBF and NO [23]. Acetylcholine released from cholinergic nerves has been reported to contribute to skin vasodilation via NO mechanism [24].…”

Nitrite and Nitric Oxide as Potential Diagnostic Markers in Acute Vascular Diseases

“…Intravascular use of NO electrodes for a prolonged period may also be limited by thrombosis. Most examples of NO electrodes in human use are limited to non-vascular applications, such as extracorporeal blood during hemodialysis [57], insertion into synovial fluid [58] and subcutaneous insertion into the forearm [59].…”