H1 but not H2 histamine receptor activation contributes to the rise in skin blood flow during whole body heating in humans

Wong, Brett J.; Wilkins, Brad W.; Minson, Christopher T.

doi:10.1113/jphysiol.2004.071779

Cited by 94 publications

(95 citation statements)

References 33 publications

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“…However, it produced a potentially important finding. Wong et al (34) showed that desensitization of neurokinin type 1 (NK 1 ) receptors decreased the response in CVC to whole body heating. This was an intriguing and provocative finding, suggesting that substance P is involved in the active vasodilator system.…”

Section: Discussionmentioning

confidence: 99%

“…LA is not typically used with microdialysis fiber placement unless sensory nerve blockade is a part of the question, because the application of LA may affect the vascular responses (5,11,15,21). Wong et al (34) recently provided evidence for an involvement of substance P in the cutaneous vascular response to whole body heat stress. Because sensory nerves are a known source for substance P, this general consideration that LA might affect the response would appear to be well founded.…”

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confidence: 99%

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The effect of microdialysis needle trauma on cutaneous vascular responses in humans

Hodges

Chiu²,

Kosiba³

et al. 2009

Journal of Applied Physiology

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The effect of microdialysis needle trauma on cutaneous vascular responses in humans. J Appl Physiol 106: 1112-1118, 2009. First published February 5, 2009 doi:10.1152/japplphysiol.91508.2008.-Microdialysis enables in-depth mechanistic study of the cutaneous circulation in humans. However, whether the insertion or presence of the microdialysis fiber (MDF) affects the skin circulation or its responses is unknown. We tested whether the cutaneous vascular response to whole body heating (WBH) was affected by MDF or by pretreatment with ice (part 1) or local anesthesia (LA; part 2). Eleven subjects participated, 9 in part 1 and 8 in part 2 (5 participated in both). In both parts, four sites on the forearm were selected, providing untreated control, MDF only, ice or LA only, and combined MDF plus ice or LA. A tube-lined suit controlled whole body skin temperature, which was raised to ϳ38°C for WBH. Skin sites were instrumented with laser-Doppler flow probes. Data were expressed as cutaneous vascular conductance (CVC). Baseline levels were not different among sites (P Ͼ 0.05). In part 1, the internal temperature for the onset of vasodilation was higher (P Ͼ 0.05) with MDF with or without ice pretreatment than at untreated control sites (control 36.6 Ϯ 0.1°C, Ice 36.5 Ϯ 0.1, MDF 36.8 Ϯ 0.1°C, and IceϩMDF 36.8 Ϯ 0.1°C). Peak CVC during WBH was decreased (P Ͻ 0.05) by MDF (control 73 Ϯ 7 vs. MDF 59 Ϯ 6% of maximal CVC). Ice (73 Ϯ 6% of maximal CVC) or IceϩMDF (69 Ϯ 6% of maximal CVC) did not affect (P Ͼ 0.05) peak CVC compared with control. In part 2, the temperature threshold for the onset of vasodilation was increased by MDF with or without LA treatment and by LA alone (P Ͻ 0.05; control 36.6 Ϯ 0.1°C, MDF 36.7 Ϯ 0.1°C, LA 36.8 Ϯ 0.1°C, and LAϩMDF 36.8 Ϯ 0.1°C). Peak CVC was decreased by MDF (control 69 Ϯ 6% of maximal CVC vs. MDF 58 Ϯ 8% of maximal CVC; P Ͻ 0.05). LA only (65 Ϯ 10% of maximal CVC) or MDF in the presence of LA (73 Ϯ 12% of maximal CVC) did not affect (P Ͼ 0.05) peak CVC compared with control. Thus LA or MDF increases the temperature threshold for the onset of vasodilation. MDF alone decreases the peak vasodilator response in CVC to WBH; however, this attenuation did not occur if ice or LA is used before MDF placement. Ice or LA alone do not affect the peak response in CVC to WBH. How those treatments prevent or reverse the effect of MDF placement is presently unclear.skin blood flow; active vasodilation; ice; local anesthesia; laserDoppler flowmetry MICRODIALYSIS IS A TECHNIQUE that over the past 20 yr has become a common procedure in humans. The first report of the in vivo use of microdialysis in humans concerned studies of the interstitial space (19). In the last decade or so, microdialysis coupled with laser-Doppler flowmetry has provided a powerful system for in-depth mechanistic analysis of how the cutaneous circulation functions in vivo. The microdialysis technique often involves insertion of a "guide," typically a 25-gauge needle, intradermally for ϳ2.5 cm before exiting. The microdialysis fiber i...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

The effect of microdialysis needle trauma on cutaneous vascular responses in humans

Hodges

Chiu²,

Kosiba³

et al. 2009

Journal of Applied Physiology

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“…The precise vasodilator(s) released from sympathetic cholinergic nerves remains unresolved; however, several vasodilators have been implicated in reflex cutaneous vasodilation, including vasoactive intestinal polypeptide (VIP) (1, 18), vasodilator prostanoids (20), H1 histamine receptors (33), and neurokinin-1 (NK 1 ) receptors (31). In addition to the aforementioned vasodilators, nitric oxide (NO) has been shown to directly contribute ϳ30 -45% to active vasodilation (14,25,28), and several sources of NO have been implicated (17,26,31,33), including neuronal NO synthase (13, 16).…”

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Transient receptor potential vanilloid type 1 channels contribute to reflex cutaneous vasodilation in humans

Wong

Fieger

2012

Journal of Applied Physiology

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Wong BJ, Fieger SM. Transient receptor potential vanilloid type 1 channels contribute to reflex cutaneous vasodilation in humans. J Appl Physiol 112: 2037-2042, 2012. First published April 19, 2012 doi:10.1152/japplphysiol.00209.2012.-Mechanisms underlying the cutaneous vasodilation in response to an increase in core temperature remain unresolved. The purpose of this study was to determine a potential contribution of transient receptor potential vanilloid type 1 (TRPV-1) channels to reflex cutaneous vasodilation. Twelve subjects were equipped with four microdialysis fibers on the ventral forearm, and each site randomly received 1) 90% propylene glycol ϩ 10% lactated Ringer (vehicle control); 2) 10 mM L-NAME; 3) 20 mM capsazepine to inhibit TRPV-1 channels; 4) combined 10 mM L-NAME ϩ 20 mM capsazepine. Whole body heating was achieved via water-perfused suits sufficient to raise oral temperature at least 0.8°C above baseline. Maximal skin blood flow was achieved by local heating to 43°C and infusion of 28 mM nitroprusside. Systemic arterial pressure (SAP) was measured, and skin blood flow was monitored via laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was calculated as LDF/SAP and normalized to maximal vasodilation (%CVC max). Capsazepine sites were significantly reduced compared with control (50 Ϯ 4%CVC max vs. 67 Ϯ 5%CVC max, respectively; P Ͻ 0.05). L-NAME (33 Ϯ 3%CVCmax) and L-NAME ϩ capsazepine (30 Ϯ 4%CVCmax) sites were attenuated compared with control (P Ͻ 0.01) and capsazepine (P Ͻ 0.05); however, there was no difference between L-NAME and combined L-NAME ϩ capsazepine. These data suggest TRPV-1 channels participate in reflex cutaneous vasodilation and TRPV-1 channels may account for a portion of the NO component. TRPV-1 channels may have a direct neural contribution or have an indirect effect via increased arterial blood temperature. Whether the TRPV-1 channels directly or indirectly contribute to reflex cutaneous vasodilation remains uncertain. microdialysis; heat stress; nitric oxide INCREASES IN SKIN BLOOD FLOW and sweating represent humans' primary physiological defense against an increase in core temperature. The initial increase in skin blood flow during hyperthermia is driven primarily by withdrawal of tonic sympathetic vasoconstrictor tone, which results in approximate doubling of resting thermoneutral skin blood flow(8, 23). Further increases in skin blood flow, concomitant with the onset of sweating, are mediated by reflex sympathetic cholinergic nerve activity (8). This reflex cutaneous active vasodilation accounts for 85-95% of the increase in skin blood flow during hyperthermia and can result in nearly 8 liters/min of cardiac output directed to the cutaneous vasculature(24).The co-transmission theory of cutaneous active vasodilation suggests acetylcholine and one or more unknown vasodilators are co-released from sympathetic cholinergic nerves, where acetylcholine is primarily responsible for the sweat response and the unknown vasodilator(s) are responsible for the refle...

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“…However, an additional prostaglandins-independent mechanism contributed to blushing during and after singing and to flushing immediately after exercise, as blood flow was greater than baseline both at the ibuprofen-treated and control sites at these points in the experiment. Possibilities include release of sympathetic vasoconstrictor tone (Drummond, 1997), active sympathetic vasodilatation (Drummond and Finch, 1999), or mediation by acetylcholine (Shibasaki et al, 2002), neuronal nitric oxide Kellogg et al, 2008), vasoactive intestinal polypeptide (Bennett et al, 2003;Kellogg et al, 2010), histamine (Wong et al, 2004), or a neurokinin receptor agonist such as substance P (Wong and Minson, 2006). Beta-adrenergic vasodilatation might also have contributed to blushing (Drummond, 1997).…”

Section: Discussionmentioning

confidence: 99%

Topical ibuprofen inhibits blushing during embarrassment and facial flushing during aerobic exercise in people with a fear of blushing

Drummond

Minosora

Little

et al. 2013

European Neuropsychopharmacology

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Cite this article as: Peter D. Drummond, Kate Minosora, Gretta Little, Wendy Keay, Topical ibuprofen inhibits blushing during embarrassment and facial flushing during aerobic exercise in people with a fear of blushing, European Neuropsychopharmacology, http://dx.doi.org/10. 1016/j.euroneuro.2013.07.013 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The flush that develops during whole-body heat stress depends partly on prostaglandins production in the skin. Variations in the strength of this local mechanism may contribute to individual differences in susceptibility to blushing and associated anxiety. To investigate this in the present study, the anti-inflammatory agent ibuprofen (which blocks prostaglandins formation) was applied topically to a small area of the cheek in 16 participants with a fear of blushing and in another 14 without this fear. Changes in skin blood flow were monitored at the ibuprofen-treated site and at a mirror image control site while participants sang (to induce embarrassment and blushing) and during aerobic exercise (to induce flushing). The topical ibuprofen treatment inhibited increases in cheek blood flow in both groups during both of these tasks. However, increases in cheek blood flow were greater in participants with high than low fear of blushing immediately after exercise. These findings suggest that prostaglandins contribute to dilatation of facial blood vessels both during emotional arousal (embarrassment) and aerobic exercise. Furthermore, fear of blushing may be associated with mechanisms that delay the resumption of normal vascular tone after a period of vasodilatation. Whether topical ibuprofen gel is suitable for intermittent or long-term use as an aid for blushing control requires further investigation.

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H1 but not H2 histamine receptor activation contributes to the rise in skin blood flow during whole body heating in humans

Cited by 94 publications

References 33 publications

The effect of microdialysis needle trauma on cutaneous vascular responses in humans

The effect of microdialysis needle trauma on cutaneous vascular responses in humans

Transient receptor potential vanilloid type 1 channels contribute to reflex cutaneous vasodilation in humans

Topical ibuprofen inhibits blushing during embarrassment and facial flushing during aerobic exercise in people with a fear of blushing

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