Cutaneous vasoconstrictor response to whole body skin cooling is altered by time of day

2003 ◽  
Vol 94 (3) ◽  
pp. 930-934 ◽  
Author(s):  
Ken Aoki ◽  
Dan P. Stephens ◽  
Adham R. Saad ◽  
John M. Johnson
Keyword(s):  
Cooling Water ◽  
Time Of Day ◽  
Whole Body ◽  
Doppler Flowmetry ◽  
Diurnal Difference ◽  
Vasoconstrictor Response ◽  
Skin Cooling ◽  
A Site ◽  
The Relationship ◽  
Cutaneous Vascular Conductance

To test for a diurnal difference in the vasoconstrictor control of the cutaneous circulation, we performed whole body skin cooling (water-perfused suits) at 0600 (AM) and 1600 (PM). After whole body skin temperature (Tsk) was controlled at 35°C for 10 min, it was progressively lowered to 32°C over 18–20 min. Skin blood flow (SkBF) was monitored by laser-Doppler flowmetry at three control sites and at a site that had been pretreated with bretylium by iontophoresis to block noradrenergic vasoconstriction. After whole body skin cooling, maximal cutaneous vascular conductance (CVC) was measured by locally warming the sites of SkBF measurement to 42°C for 30 min. Before whole body skin cooling, sublingual temperature (Tor) in the PM was significantly higher than that in the AM ( P < 0.05), but CVC, expressed as a percentage of maximal CVC (%CVCmax), was not statistically different between AM and PM. During whole body skin cooling, %CVCmax levels at bretylium-treated sites in AM or PM were not significantly reduced from baseline. In the PM, %CVCmax at control sites fell significantly at Tsk of 34.3 ± 0.01°C and lower ( P< 0.05). In contrast, in the AM %CVCmax at control sites was not significantly reduced from baseline until Tskreached 32.3 ± 0.01°C and lower ( P < 0.05). Furthermore, the decrease in %CVCmax in the PM was significantly greater than that in AM at Tsk of 33.3 ± 0.01°C and lower ( P < 0.05). Integrative analysis of the CVC response with respect to both Tor and Tsk showed that the cutaneous vasoconstrictor response was shifted to higher internal temperatures in the PM. These findings suggest that during whole body skin cooling the reflex control of the cutaneous vasoconstrictor system is shifted to a higher internal temperature in the PM. Furthermore, the slope of the relationship between CVC and Tsk is steeper in the PM compared with that in the AM.

Reflex control of cutaneous vasoconstrictor system is reset by exogenous female reproductive hormones

1999 ◽  
Vol 87 (1) ◽  
pp. 381-385 ◽  
Author(s):  
Nisha Charkoudian ◽  
John M. Johnson
Keyword(s):  
Contraceptive Use ◽  
Reproductive Hormones ◽  
Doppler Flowmetry ◽  
Oral Contraceptive Use ◽  
Vasoconstrictor Response ◽  
Reflex Control ◽  
Relationship Of ◽  
The Relationship ◽  
Cutaneous Vascular Conductance ◽  
Cutaneous Vasoconstriction

To determine whether cardiovascular influences of exogenous female steroid hormones include effects on reflex thermoregulatory control of the adrenergic cutaneous vasoconstrictor system, we conducted ramp decreases in skin temperature (Tsk) in eight women in both high- and low (placebo)-progesterone/estrogen phases of oral contraceptive use. With the use of water-perfused suits, Tsk was held at 36°C for 10 min (to minimize initial vasoconstrictor activity) and was then decreased in a ramp, ∼0.2°C/min for 12–15 min. Subjects rested supine for 30–40 min before each experiment, and the protocol was terminated before the onset of shivering. Skin blood flow was monitored by laser-Doppler flowmetry and arterial pressure by finger photoplethysmography. In all experiments, cutaneous vasoconstriction began immediately with the onset of cooling, and cutaneous vascular conductance (CVC) decreased progressively with decreasing Tsk. Regression analysis of the relationship of CVC to Tsk showed no difference in slope between phases (low-hormone phase: 17.67 ± 5.57; high-hormone phase: 17.40 ± 8.00 %baseline/°C; P > 0.05). Additional studies involving local blockade confirmed this response as being solely due to the adrenergic vasoconstrictor system. Waking oral temperature (Tor) was significantly higher on high-hormone vs. low-hormone days (36.60 ± 0.11 vs. 36.37 ± 0.09 °C, respectively; P < 0.02). Integrative analysis of CVC in terms of simultaneous values for Tsk and Tor showed that the cutaneous vasoconstrictor response was shifted in the high-hormone phase such that a higher Tor was maintained throughout cooling ( P < 0.05). Thus reflex thermoregulatory control of the cutaneous vasoconstrictor system is shifted to higher internal temperatures by exogenous female reproductive hormones.

Relative roles of local and reflex components in cutaneous vasoconstriction during skin cooling in humans

2006 ◽  
Vol 100 (6) ◽  
pp. 2083-2088 ◽  
Author(s):  
Guy E. Alvarez ◽  
Kun Zhao ◽  
Wojciech A. Kosiba ◽  
John M. Johnson
Keyword(s):  
Reflex Response ◽  
Whole Body ◽  
Local Cooling ◽  
Doppler Flowmetry ◽  
Peltier Cooler ◽  
Vasoconstrictor Response ◽  
Skin Cooling ◽  
Body Cooling ◽  
Whole Body Cooling ◽  
Independent Effects

The reduction in skin blood flow (SkBF) with cold exposure is partly due to the reflex vasoconstrictor response from whole body cooling (WBC) and partly to the direct effects of local cooling (LC). Although these have been examined independently, little is known regarding their roles when acting together, as occurs in environmental cooling. We tested the hypothesis that the vasoconstrictor response to combined LC and WBC would be additive, i.e., would equal the sum of their independent effects. We further hypothesized that LC would attenuate the reflex vasoconstrictor response to WBC. We studied 16 (7 women, 9 men) young (30.5 ± 2 yr) healthy volunteers. LC and WBC were accomplished with metal Peltier cooler-heater probe holders and water-perfused suits, respectively. Forearm SkBF was monitored by laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was calculated as LDF/blood pressure. Subjects underwent 15 min of LC alone or 15 min of WBC with and without simultaneous LC, either at equal levels (34–31°C) or as equipotent stimuli (34–28°C LC; 34–31°C WBC). The fall in CVC with combined WBC and LC was greater ( P < 0.05) than for either alone (57.0 ± 5% combined vs. 39.2 ± 6% WBC; 34.4 ± 4% LC) with equipotent cooling, but it was only significantly greater than for LC alone with equal levels of cooling (51.3 ± 8% combined vs. 29.5 ± 4% LC). The sum of the independent effects of WBC and LC was greater than their combined effects (74.9 ± 4 vs. 51.3 ± 8% equal and 73.6 ± 7 vs. 57.0 ± 5% equipotent; P < 0.05). The fall in CVC with WBC at LC sites was reduced compared with control sites (17.6 ± 2 vs. 42.4 ± 8%; P < 0.05). Hence, LC contributes importantly to the reduction in SkBF with body cooling, but also suppresses the reflex response, resulting in a nonadditive effect of these two components.

The role of baseline in the cutaneous vasoconstrictor responses during combined local and whole body cooling in humans

2007 ◽  
Vol 293 (5) ◽  
pp. H3187-H3192 ◽  
Author(s):  
Gary J. Hodges ◽  
Wojciech A. Kosiba ◽  
Kun Zhao ◽  
Guy E. Alvarez ◽  
John M. Johnson
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Laser Doppler ◽  
Whole Body ◽  
Local Cooling ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Body Cooling ◽  
Whole Body Cooling

Previous work showed that local cooling (LC) attenuates the vasoconstrictor response to whole body cooling (WBC). We tested the extent to which this attenuation was due to the decreased baseline skin blood flow following LC. In eight subjects, skin blood flow was assessed using laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was expressed as LDF divided by blood pressure. Subjects were dressed in water-perfused suits to control WBC. Four forearm sites were prepared with microdialysis fibers, local heating/cooling probe holders, and laser-Doppler probes. Three sites were locally cooled from 34 to 28°C, reducing CVC to 45.9 ± 3.9, 42 ± 3.9, and 44.5 ± 4.8% of baseline ( P < 0.05 vs. baseline; P > 0.05 among sites). At two sites, CVC was restored to precooling baseline levels with sodium nitroprusside (SNP) or isoproterenol (Iso), increasing CVC to 106.4 ± 12.4 and 98.9 ± 10.1% of baseline, respectively ( P > 0.05 vs. precooling). Whole body skin temperature, apart from the area of blood flow measurement, was reduced from 34 to 31°C. Relative to the original baseline, CVC decreased ( P < 0.05) by 44.9 ± 2.8 (control), 11.3 ± 2.4 (LC only), 29 ± 3.7 (SNP), and 45.8 ± 8.7% (Iso). The reductions at LC only and SNP sites were less than at control or Iso sites ( P < 0.05); the responses at those latter sites were not different ( P > 0.05), suggesting that the baseline change in CVC with LC is important in the attenuation of reflex vasoconstrictor responses to WBC.

Oral vitamin C enhances the adrenergic vasoconstrictor response to local cooling in human skin

2012 ◽  
Vol 112 (10) ◽  
pp. 1689-1697 ◽  
Author(s):  
Fumio Yamazaki
Keyword(s):  
Human Skin ◽  
Local Administration ◽  
Adrenergic System ◽  
Local Cooling ◽  
Oral Vitamin ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Forearm Skin ◽  
Cutaneous Vascular Conductance

Local administration of ascorbic acid (Asc) at a supraphysiological concentration inhibits the cutaneous vasoconstrictor response to local cooling (LC). However, whether orally ingesting Asc inhibits the LC-induced vasoconstrictor response remains unknown. The purpose of the present study was to examine the acute influence of oral Asc on the adrenergic vasoconstrictor response to LC in human skin. In experiment 1, skin blood flow (SkBF) was measured by laser-Doppler flowmetry at three sites (forearm, calf, palm). The three skin sites were locally cooled from 34 to 24°C at −1°C/min and maintained at 24°C for 20 min before (Pre) and 1.5 h after (Post) oral Asc (2-g single dose) or placebo supplementation. Cutaneous vascular conductance (CVC) was calculated as the ratio of SkBF to blood pressure and expressed relative to the baseline value before LC. Oral Asc enhanced ( P < 0.05) the reductions in CVC in the forearm (Pre, −50.3 ± 3.3%; Post, −57.8 ± 2.2%), calf (Pre, −52.6 ± 3.7%; Post, −66.1 ± 4.3%), and palm (Pre, −46.2 ± 6.2%; Post, −60.4 ± 5.6%) during LC. The placebo did not change the responses at any site. In experiment 2, to examine whether the increased vasoconstrictor response caused by oral Asc is due to the adrenergic system, the release of neurotransmitters from adrenergic nerves in forearm skin was blocked locally by iontophoresis of bretylium tosylate (BT). Oral Asc enhanced ( P < 0.05) the reductions in CVC at untreated control sites but did not change the responses at BT-treated sites during LC. In experiment 3, to further examine whether adrenergically mediated vasoconstriction is enhanced by oral Asc, 0.1 mM tyramine was administered using intradermal microdialysis in the forearm skin at 34°C in the Pre and Post periods. Oral Asc increased ( P < 0.05) the tyramine-induced reduction in CVC. These findings suggest that oral Asc acutely enhances the cutaneous vasoconstrictor responses to LC through the modification of adrenergic sympathetic mechanisms.

Limb-specific differences in the skin vascular responsiveness to adrenergic agonists

2011 ◽  
Vol 111 (1) ◽  
pp. 170-176 ◽  
Author(s):  
Fumio Yamazaki ◽  
Nagisa Yuge
Keyword(s):  
Regional Differences ◽  
Minor Role ◽  
Adrenergic Agonists ◽  
Drug Infusion ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Vascular Responsiveness ◽  
A Minor ◽  
Cutaneous Vascular Conductance

In this study, to test the hypothesis that adrenergic vasoconstrictor responses of the legs are greater compared with the arms in human skin, cutaneous vascular conductance (CVC) in the forearm and calf were compared during the infusion of adrenergic agonists in healthy young volunteers. Under normothermic conditions, norepinephrine (NE, α- and β-agonist, 1 × 10−8 to 1 × 10−2 M), phenylephrine (PHE, α1-agonist, 1 × 10−8 to 1 × 10−2 M), dexmedetomidine (DEX, α2-agonist, 1 × 10−9 to 1 × 10−4 M), and isoproterenol (ISO, β-agonist, 1 × 10−8 to 1 × 10−3 M) were administered by intradermal microdialysis. Skin blood flow (SkBF) was measured by laser-Doppler flowmetry, and the local temperature at SkBF-measuring sites was maintained at 34°C throughout the experiments. CVC was calculated as the ratio of SkBF to blood pressure and expressed relative to the baseline value before drug infusion. The dose of NE at the onset of vasoconstriction and the effective dose (ED50) resulting in 50% of the maximal vasoconstrictor response for NE were lower ( P < 0.001) in the calf than forearm. The ED50 for PHE and DEX was also lower ( P < 0.05) in the calf than forearm. Increases in CVC in response to ISO were potentially smaller in the calf, but the statistical differences in the responses were dependent on the expressions of CVC. These findings suggest that the cutaneous vasoconstrictor responsiveness to exogenous NE is greater in the legs than in the arms due to a higher α1- and α2-adrenoceptor reactivity, while the β-adrenoceptor function plays a minor role in regional differences in adrenergic vasoconstriction in normothermic humans.

scholarly journals Diurnal variation in cutaneous vasodilator and vasoconstrictor systems during heat stress

2001 ◽  
Vol 281 (2) ◽  
pp. R591-R595 ◽  
Author(s):  
Ken Aoki ◽  
Dan P. Stephens ◽  
John M. Johnson
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Diurnal Variation ◽  
Skin Blood Flow ◽  
Whole Body ◽  
Noninvasive Blood Pressure ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Cutaneous Vascular Conductance

It is not clear whether the diurnal variation in the cutaneous circulatory response to heat stress is via the noradrenergic vasoconstrictor system or the nonadrenergic active vasodilator system. We conducted whole body heating experiments in eight male subjects at 0630 (AM) and 1630 (PM). Skin blood flow was monitored by laser-Doppler flowmetry at control sites and at sites pretreated with bretylium (BT) to block noradrenergic vasoconstriction. Noninvasive blood pressure was used to calculate cutaneous vascular conductance. The sublingual temperature (Tor) threshold for cutaneous vasodilation was significantly higher in PM at control and at BT-treated sites (both P < 0.01), suggesting the diurnal shift in threshold depends on the active vasodilator system. The slope of cutaneous vascular conductance as a percentage of its maximum with respect to Tor was significantly lower in AM at control sites only. Also, in the AM, the slope at control sites was significantly lower than that at BT-treated sites ( P < 0.05), suggesting that the diurnal change in the sensitivity of cutaneous vasodilation depends on vasoconstrictor system function. Overall, the diurnal variation in the reflex control of skin blood flow during heat stress involves both vasoconstrictor and active vasodilator systems.

Influence of hyperoxia on skin vasomotor control in normothermic and heat-stressed humans

2007 ◽  
Vol 103 (6) ◽  
pp. 2026-2033 ◽  
Author(s):  
Fumio Yamazaki ◽  
Kazuo Takahara ◽  
Ryoko Sone ◽  
John M. Johnson
Keyword(s):  
Thermal Conditions ◽  
Inhibitory Effects ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Forearm Skin ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Cutaneous Vascular Conductance ◽  
Male Subjects ◽  
Cutaneous Vasoconstriction

Hyperoxia induces skin vasoconstriction in humans, but the mechanism is still unclear. In the present study we examined whether the vasoconstrictor response to hyperoxia is through activated adrenergic function ( protocol 1) or through inhibitory effects on nitric oxide synthase (NOS) and/or cyclooxygenase (COX) ( protocol 2). We also tested whether any such vasoconstrictor effect is altered by body heating. In protocol 1 ( n = 11 male subjects), release of norepinephrine from adrenergic terminals in the forearm skin was blocked locally by iontophoresis of bretylium (BT). In protocol 2, the NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME) and the nonselective COX antagonist ketorolac (Keto) were separately administered by intradermal microdialysis in 11 male subjects. In the two protocols, subjects breathed 21% (room air) or 100% O2 in both normothermia and hyperthermia. Skin blood flow (SkBF) was monitored by laser-Doppler flowmetry. Cutaneous vascular conductance (CVC) was calculated as the ratio of SkBF to blood pressure measured by Finapres. In protocol 1, breathing 100% O2 decreased ( P < 0.05) CVC at the BT-treated and at untreated sites from the levels of CVC during 21% O2 breathing both in normothermia and hyperthermia. In protocol 2, the administration of l-NAME inhibited ( P < 0.05) the reduction of CVC during 100% O2 breathing in both thermal conditions. The administration of Keto inhibited ( P < 0.05) the reduction of CVC during 100% O2 breathing in hyperthermia but not in normothermia. These results suggest that skin vasoconstriction with hyperoxia is partly due to the decreased activity of functional NOS in normothermia and hyperthermia. We found no significant role for adrenergic mechanisms in hyperoxic vasoconstriction. Decreased production of vasodilator prostaglandins may play a role in hyperoxia-induced cutaneous vasoconstriction in heat-stressed humans.

Role of sensory nerves in the cutaneous vasoconstrictor response to local cooling in humans

2007 ◽  
Vol 293 (1) ◽  
pp. H784-H789 ◽  
Author(s):  
Gary J. Hodges ◽  
J. Andrew Traeger ◽  
Tri Tang ◽  
Wojciech A. Kosiba ◽  
Kun Zhao ◽  
...  
Keyword(s):  
Sensory Nerve ◽  
Sensory Nerves ◽  
Nerve Function ◽  
Local Cooling ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Cutaneous Vascular Conductance ◽  
Term Response

Local cooling (LC) causes a cutaneous vasoconstriction (VC). In this study, we tested whether there is a mechanism that links LC to VC nerve function via sensory nerves. Six subjects participated. Local skin and body temperatures were controlled with Peltier probe holders and water-perfused suits, respectively. Skin blood flow at four forearm sites was monitored by laser-Doppler flowmetry with the following treatments: untreated control, pretreatment with local anesthesia (LA) blocking sensory nerve function, pretreatment with bretylium tosylate (BT) blocking VC nerve function, and pretreatment with both LA and BT. Local skin temperature was slowly reduced from 34 to 29°C at all four sites. Both sites treated with LA produced an increase in cutaneous vascular conductance (CVC) early in the LC process (64 ± 55%, LA only; 42 ± 14% LA plus BT; P < 0.05), which was absent at the control and BT-only sites (5 ± 8 and 6 ± 8%, respectively; P > 0.05). As cooling continued, there were significant reductions in CVC at all sites ( P < 0.05). At control and LA-only sites, CVC decreased by 39 ± 4 and 46 ± 8% of the original baseline values, which were significantly ( P < 0.05) more than the reductions in CVC at the sites treated with BT and BT plus LA (−26 ± 8 and −22 ± 6%). Because LA affected only the short-term response to LC, either alone or in the presence of BT, we conclude that sensory nerves are involved early in the VC response to LC, but not for either adrenergic or nonadrenergic VC with longer term LC.

scholarly journals Reflex control of the cutaneous circulation after acute and chronic local capsaicin

2001 ◽  
Vol 90 (5) ◽  
pp. 1860-1864 ◽  
Author(s):  
Nisha Charkoudian ◽  
Bérengère Fromy ◽  
Jean-Louis Saumet
Keyword(s):  
Whole Body ◽  
Vascular Conductance ◽  
Sensory Afferents ◽  
Doppler Flowmetry ◽  
Local Activity ◽  
Vasodilator Response ◽  
Temperature Thresholds ◽  
Local Warming ◽  
Topical Capsaicin ◽  
Cutaneous Vascular Conductance

To investigate whether local activity of capsaicin-sensitive sensory afferents in the skin has a modulatory role in the reflex cutaneous vasodilator response to hyperthermia in humans, experiments were conducted in two parts. First, low-dose topical capsaicin (0.025%) was administered acutely to stimulate local activity of these afferents. Second, we temporarily desensitized these nerves in a small area of skin using chronic capsaicin treatment (0.075% for 7 days). Each intervention was followed by whole body heating using water-perfused suits and then by local warming to 42°C for assessment of maximum cutaneous vascular conductance. Skin blood flow was measured by laser-Doppler flowmetry and divided by mean arterial pressure (Finapres) for assessment of cutaneous vascular conductance. Maximum vascular conductance was not influenced by either acute or chronic capsaicin treatment ( P > 0.10). After acute capsaicin, baseline cutaneous vascular conductance was elevated above that at control sites (25.34 ± 6.25 vs. 10.57 ± 2.42%max; P < 0.05). However, internal temperature thresholds for vasodilation were not affected by either acute or chronic capsaicin ( P > 0.10). Furthermore, neither acute (control: 112.74 ± 36.83 vs. acute capsaicin: 96.92 ± 28.92%max/°C; P > 0.10) nor chronic (control: 142.45 ± 61.89 vs. chronic capsaicin: 132.12 ± 52.60%max/°C; P > 0.10) capsaicin administration influenced the sensitivity of the reflex cutaneous vasodilator response. We conclude that local activity of capsaicin-sensitive afferents in the skin does not modify reflex cutaneous vasodilation during hyperthermia.

Competition between cutaneous active vasoconstriction and active vasodilation during exercise in humans

1991 ◽  
Vol 261 (4) ◽  
pp. H1184-H1189 ◽  
Author(s):  
D. L. Kellogg ◽  
J. M. Johnson ◽  
W. A. Kosiba
Keyword(s):  
Cold Stress ◽  
Whole Body ◽  
Strenuous Exercise ◽  
Doppler Flowmetry ◽  
Flow Monitoring ◽  
Vasodilator Activity ◽  
Cutaneous Vascular Conductance ◽  
Male Subjects ◽  
Cutaneous Vasoconstriction ◽  
Body Heat

Cutaneous vasoconstriction occurs in response to the initiation of dynamic exercise in hyperthermia. To find whether this response was due to increased vasoconstrictor activity or to withdrawal of active vasodilator activity, blood flow monitoring with laser-Doppler flowmetry (LDF) was combined with the local iontophoresis of bretylium. Each of six male subjects had two forearm sites treated with bretylium for selective local blockade of noradrenergic vasoconstrictor nerves in skin. LDF was monitored at those sites and at two adjacent untreated sites. Mean arterial pressure (MAP) was measured, and cutaneous vascular conductance (CVC) was calculated as LDF/MAP. After iontophoresis, subjects underwent 3 min of cold stress (water-perfused suits) to verify vasoconstrictor blockade. CVC at untreated sites fell by 35.9 +/- 3.1% (P less than 0.01) and at bretylium-treated sites was not significantly changed (P greater than 0.10). During strenuous exercise in normothermia, CVC at untreated sites fell by 16.1 +/- 4.1% (P less than 0.05) and was unchanged at bretylium-treated sites (+12.7 +/- 6.6%, P greater than 0.05). Whole body heat stress was then applied. When exercise was repeated in hyperthermia, CVC at untreated sites fell by 11.6 +/- 3.8% (P less than 0.05) but was not significantly changed at bretylium-treated sites (+3.6 +/- 3.0%, P greater than 0.30). Following return to normothermia, cold stress verified the persistence of the blockade. We conclude that exercise initiation causes a cutaneous vasoconstriction largely or entirely due to enhanced active vasoconstrictor tone in both normothermia and hyperthermia. Little or no role in this response can be ascribed to reduced active vasodilator activity.

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