Two neural mechanisms for respiration-induced cutaneous vasodilatation in humans

Citation
Bg. Wallin et al., Two neural mechanisms for respiration-induced cutaneous vasodilatation in humans, J PHYSL LON, 513(2), 1998, pp. 559-569
Citations number
25
Categorie Soggetti
Physiology
Journal title
JOURNAL OF PHYSIOLOGY-LONDON
ISSN journal
00223751 → ACNP
Volume
513
Issue
2
Year of publication
1998
Pages
559 - 569
Database
ISI
SICI code
0022-3751(199812)513:2<559:TNMFRC>2.0.ZU;2-1
Abstract
1. In humans, a deep breath is known to induce cutaneous vasoconstriction i n the warm state, and vasodilatation in the cold state. To investigate whet her vasodilatation in the cold state is related to reduction of sympathetic vasoconstrictor nerve traffic, we studied the effect of a deep breath on v ascular resistance in a skin area on the dorsum of the hand, in which relea se of noradrenaline from sympathetic nerves was blocked by iontophoretic pr etreatment with bretylium tosylate. Simultaneous measurements were made in two control areas. In eight healthy subjects, data were obtained from deep breaths taken before bretylium in the warm state, after general cooling to a finger skin temperature below 25 degrees C and after rewarming to above 3 2 degrees C. 2. In the warm state before bretylium pretreatment, the deep breath evoked short-lasting vasoconstrictions at all sites. In the cold state there was n o change of vascular resistance in the bretylium-pretreated area, whereas i n the control areas an initial tendency towards vasoconstriction was follow ed by a significant transient vasodilatation. After rewarming, transient va soconstrictions reappeared at the control sites, whereas only a transient v asodilatation occurred at the bretylium-pretreated site. 3. In six healthy subjects we also monitored the effects of a deep breath o n skin sympathetic nerve activity (recorded by microneurography in the pero neal nerve), and skin vascular resistance within the innervation zone of th e impaled nerve fascicle in the foot. Data from thirty deep breaths per sub ject were averaged. 4. In the cold state, the deep breath induced a strong increase in neural d ischarge, followed by a transient reduction of nerve traffic lasting approx imately 15 s and associated with a subsequent reduction of vascular resista nce. 5. We conclude that the deep breath-induced vasodilatation in the cold stat e is due to reduction of sympathetic vasoconstrictor nerve traffic. The vas odilatation after bretylium treatment in the warm state raises the possibil ity that a deep breath induces two simultaneous neural reactions, a vasocon strictor and an active vasodilator component, the latter being weaker and n ormally masked by the strong vasoconstrictor component.