Effect of high local temperature on reflex cutaneous vasodilation

1984 ◽  
Vol 57 (1) ◽  
pp. 191-196 ◽  
Author(s):  
W. F. Taylor ◽  
J. M. Johnson ◽  
D. O'Leary ◽  
M. K. Park
Keyword(s):  
Blood Flow ◽  
Whole Body ◽  
Ambient Conditions ◽  
Basal Tone ◽  
Forearm Skin ◽  
Local Warming ◽  
C 30 ◽  
Average Rise ◽  
Reflex Cutaneous Vasodilation ◽  
Body Heat

We examined the effect of high local forearm skin temperature (Tloc) on reflex cutaneous vasodilator responses to elevated whole-body skin (Tsk) and internal temperatures. One forearm was locally warmed to 42 degrees C while the other was left at ambient conditions to determine if a high Tloc could attenuate or abolish reflex vasodilation. Forearm blood flow (FBF) was monitored in both arms, increases being indicative of increases in skin blood flow (SkBF). In one protocol, Tsk was raised to 39–40degrees C 30 min after Tloc in one arm had been raised to 42 degrees C. In a second protocol, Tsk andTloc were elevated simultaneously. In protocol 1, the locally warmed arm showed little or no change in blood flow in response to increasing Tsk and esophageal temperature (average rise = 0.76 +/-1.18 ml X 100 ml-1 X min-1), whereas FBF in the normothermic arm rose by an average of 8.84 +/- 3.85 ml X 100 ml-1 X min-1. In protocol 2, FBF in the normothermic arm converged with that in the warmed arm in three of four cases but did not surpass it. We conclude that local warming to 42 degrees C for 35–55 min prevents reflex forearm cutaneous vasodilator responses to whole-body heat stress. The data strongly suggest that this attenuation is via reduction or abolition of basal tone in the cutaneous arteriolar smooth muscle and that at a Tloc of 42 degrees C a maximum forearm SkBF has been achieved. Implicit in this conclusion is that local warming has been applied for a duration sufficient to achieve a plateau in FBF.

scholarly journals Roles of nitric oxide synthase isoforms in cutaneous vasodilation induced by local warming of the skin and whole body heat stress in humans

2009 ◽  
Vol 107 (5) ◽  
pp. 1438-1444 ◽  
Author(s):  
Dean L. Kellogg ◽  
Joan L. Zhao ◽  
Yubo Wu
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
No Synthase ◽  
Whole Body ◽  
Doppler Flowmetry ◽  
Vasodilator Response ◽  
Cutaneous Vasodilation ◽  
Forearm Skin ◽  
Whole Body Heat Stress ◽  
Body Heat

Nitric oxide (NO) participates in the cutaneous vasodilation caused by increased local skin temperature (Tloc) and whole body heat stress in humans. In forearm skin, endothelial NO synthase (eNOS) participates in vasodilation due to elevated Tloc and neuronal NO synthase (nNOS) participates in vasodilation due to heat stress. To explore the relative roles and interactions of these isoforms, we examined the effects of a relatively specific eNOS inhibitor, Nω-amino-l-arginine (LNAA), and a specific nNOS inhibitor, Nω-propyl-l-arginine (NPLA), both separately and in combination, on skin blood flow (SkBF) responses to increased Tloc and heat stress in two protocols. In each protocol, SkBF was monitored by laser-Doppler flowmetry (LDF) and mean arterial pressure (MAP) by Finapres. Cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Intradermal microdialysis was used to treat one site with 5 mM LNAA, another with 5 mM NPLA, a third with combined 5 mM LNAA and 5 mM NPLA (Mix), and a fourth site with Ringer only. In protocol 1, Tloc was controlled with combined LDF/local heating units. Tloc was increased from 34°C to 41.5°C to cause local vasodilation. In protocol 2, after a period of normothermia, whole body heat stress was induced (water-perfused suits). At the end of each protocol, all sites were perfused with 58 mM nitroprusside to effect maximal vasodilation for data normalization. In protocol 1, at Tloc = 34°C, CVC did not differ between sites ( P > 0.05). LNAA and Mix attenuated CVC increases at Tloc = 41.5°C to similar extents ( P < 0.05, LNAA or Mix vs. untreated or NPLA). In protocol 2, in normothermia, CVC did not differ between sites ( P > 0.05). During heat stress, NPLA and Mix attenuated CVC increases to similar extents, but no significant attenuation occurred with LNAA ( P < 0.05, NPLA or Mix vs. untreated or LNAA). In forearm skin, eNOS mediates the vasodilator response to increased Tloc and nNOS mediates the vasodilator response to heat stress. The two isoforms do not appear to interact during either response.

Interactions between local and reflex influences on human forearm skin blood flow

1976 ◽  
Vol 41 (6) ◽  
pp. 826-831 ◽  
Author(s):  
J. M. Johnson ◽  
G. L. Brengelmann ◽  
L. B. Rowell
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Forearm Blood Flow ◽  
Lower Body Negative Pressure ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Vasoconstrictor Response ◽  
Human Forearm ◽  
Forearm Skin ◽  
Forearm Muscle

A three-part experiment was designed to examine interactions between local and reflex influences on forearm skin blood flow (SkBF). In part I locally increasing arm skin temperature (Tsk) to 42.5 degrees C was not associated with increases in underlying forearm muscle blood flow, esophageal temperature (Tes), or forearm blood flow in the contralateral cool arm. In part II whole-body Tsk was held at 38 or 40 degrees C and the surface temperature of one arm held at 38 or 42 degrees C for prolonged periods. SkBF in the heated arm rose rapidly with the elevation in body Tsk and arm Tsk continued to rise as Tes rose. SkBF in the arm kept at 32 degrees C paralleled rising Tes. In six studies, SkBF in the cool arm ultimately converged with SkBF in the heated arm. In eight other studies, heated arm SkBF maintained an offset above cool arm SkBF throughout the period of whole-body heating. In part III, local arm Tsk of 42.5 degrees C did not abolish skin vasoconstrictor response to lower body negative pressure. We conclude that local and reflex influences to skin interact so as to modify the degree but not the pattern of skin vasomotor response.

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

2012 ◽  
Vol 112 (12) ◽  
pp. 2037-2042 ◽  
Author(s):  
Brett J. Wong ◽  
Sarah M. Fieger
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Whole Body ◽  
Transient Receptor Potential Vanilloid ◽  
Cutaneous Vasodilation ◽  
Transient Receptor ◽  
Reflex Cutaneous Vasodilation

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 + 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 + 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 (%CVCmax). Capsazepine sites were significantly reduced compared with control (50 ± 4%CVCmax vs. 67 ± 5%CVCmax, respectively; P < 0.05). l-NAME (33 ± 3%CVCmax) and l-NAME + capsazepine (30 ± 4%CVCmax) sites were attenuated compared with control ( P < 0.01) and capsazepine ( P < 0.05); however, there was no difference between l-NAME and combined l-NAME + 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.

Free-swimming swordfish, Xiphias gladius, alter the rate of whole body heat transfer: morphological and physiological specializations for thermoregulation

2017 ◽  
Vol 75 (2) ◽  
pp. 858-870 ◽  
Author(s):  
Ashley Stoehr ◽  
Joshua St. Martin ◽  
Scott Aalbers ◽  
Chugey Sepulveda ◽  
Diego Bernal
Keyword(s):  
Heat Transfer ◽  
Blood Flow ◽  
Whole Body ◽  
Vertical Movements ◽  
Pelagic Fishes ◽  
Xiphias Gladius ◽  
Flow Pathways ◽  
Body Heat ◽  
Transfer Models

Abstract Swordfish (Xiphias gladius) are large, highly-migratory pelagic, fishes that make diel, vertical excursions from the warm, surface layer (e.g. 18–24 °C) to the cold waters (∼8 °C) below the thermocline (300–600 m). They possess anatomical traits [e.g. medial red muscle (RM) position and an associated vascular rete] that could enable metabolic heat-retention and result in RM temperature elevation above ambient, or RM endothermy. We herein provide: (i) expanded anatomical descriptions of the RM-associated vasculature (i.e. central rete and lateral blood vessels), (ii) new measurements of in vivo temperature, and (iii) heat transfer models to assess the capacities for RM endothermy and physiological thermoregulation during vertical movements. Despite the presence of a medial RM and two associated blood-flow pathways (one of which forms a rete), swordfish exhibited a limited capacity for RM endothermy, with muscle temperatures approaching ambient during prolonged periods above or below the thermocline. Our heat transfer models suggest, however, that swordfish may control rates of heat loss or gain during vertical movements, possibly by altering the route of blood flow supplying the RM. Such physiological thermoregulation likely contributes to the ability of swordfish to capitalize on food resources below the thermocline, which are out of range for most other active, pelagic fishes.

Mechanisms of control of skin blood flow during prolonged exercise in humans

1993 ◽  
Vol 265 (2) ◽  
pp. H562-H568 ◽  
Author(s):  
D. L. Kellogg ◽  
J. M. Johnson ◽  
W. L. Kenney ◽  
P. E. Pergola ◽  
W. A. Kosiba
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Sweat Rate ◽  
Bicycle Ergometer ◽  
Dew Point ◽  
Whole Body ◽  
Internal Temperature ◽  
Vasodilator Activity ◽  
Forearm Skin ◽  
Reduced Rate

Exercise in a warm environment raises internal temperature and leads to a rapid increase in skin blood flow (SkBF). As exercise continues, and internal temperature approaches 38 degrees C, the rate of rise of SkBF is markedly attenuated despite further significant increases in internal temperature. To find whether this attenuation is mediated by increased cutaneous active vasoconstrictor activity or by a reduced rate of rise of active vasodilator activity, each of 12 male subjects had 0.64 cm2 forearm skin sites iontophoretically treated with bretylium tosylate for selective local blockade of noradrenergic vasoconstrictor nerves. SkBF was monitored there and at adjacent untreated control sites by laser-Doppler blood flowmetry (LDF). Whole body skin temperature (Tsk) was controlled by water-perfused suits, and esophageal temperature (Tes) was monitored as an index of internal temperature. Mean arterial pressure (MAP) was monitored and cutaneous vascular conductance was calculated as LDF/MAP. Sweat rate was also monitored by dew point hygrometry in 11 subjects. Tsk was raised to 38 degrees C, after which subjects began 20-30 min of exercise on a bicycle ergometer. The rate of the initial rapid increase in SkBF with increasing Tes was not altered by bretylium treatment (P > 0.05 between sites). The attenuation of the rate of rise during the latter phase of exercise was not abolished by bretylium treatment (P > 0.05 between sites); instead, there was a trend for the attenuation to be enhanced at those sites. We conclude that the attenuated rate of rise of SkBF is due to limitation of active vasodilator activity and not due to increased vasoconstrictor tone.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effect of whole body heat stress on peripheral vasoconstriction during leg dependency

2009 ◽  
Vol 107 (6) ◽  
pp. 1704-1709 ◽  
Author(s):  
R. Matthew Brothers ◽  
Jonathan E. Wingo ◽  
Kimberly A. Hubing ◽  
Juan Del Coso ◽  
Craig G. Crandall
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Pressure Control ◽  
Whole Body ◽  
Doppler Flowmetry ◽  
Local Mechanism ◽  
Whole Body Heat Stress ◽  
The Absolute ◽  
Absolute Decrease ◽  
Body Heat

The venoarteriolar response (VAR) increases vascular resistance upon increases in venous transmural pressure in cutaneous, subcutaneous, and muscle vascular beds. During orthostasis, it has been proposed that up to 45% of the increase in systemic vascular tone is due to VAR-related local mechanism(s). The objective of this project was to test the hypothesis that heat stress attenuates VAR-mediated cutaneous and whole leg vasoconstriction. During normothermic conditions, measurements of cutaneous blood flow (laser-Doppler flowmetry) and femoral artery blood flow (Doppler ultrasound) were obtained from both legs during supine and leg-dependent conditions. These measurements were repeated following a whole body heat stress (increase in internal temperature of 1.4 ± 0.2°C). Before leg dependency, cutaneous (CVC) and femoral vascular conductances (FVC) were significantly elevated in both legs during heat stress relative to normothermia ( P < 0.001). During leg dependency the absolute decrease in CVC was attenuated during heat stress ( P < 0.01) while the absolute decrease in FVC was unaffected ( P = 0.90). When CVC and FVC data were analyzed as a relative change from their respective baseline values, heat stress significantly attenuated the magnitude of vasoconstriction due to leg dependency in the cutaneous and femoral circulations ( P < 0.001 for both variables). These data suggest that an attenuated local vasoconstriction, evoked via the venoarteriolar response, may contribute to reduced blood pressure control and thus reduced orthostatic tolerance that occurs in heat-stressed individuals.

scholarly journals Antagonism of soluble guanylyl cyclase attenuates cutaneous vasodilation during whole body heat stress and local warming in humans

2011 ◽  
Vol 110 (5) ◽  
pp. 1406-1413 ◽  
Author(s):  
Dean L. Kellogg ◽  
Joan L. Zhao ◽  
Yubo Wu ◽  
John M. Johnson
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Guanylyl Cyclase ◽  
Soluble Guanylyl Cyclase ◽  
Whole Body ◽  
Local Skin ◽  
Cutaneous Vasodilation ◽  
Local Skin Temperature ◽  
Whole Body Heat Stress ◽  
Body Heat

We hypothesized that nitric oxide activation of soluble guanylyl cyclase (sGC) participates in cutaneous vasodilation during whole body heat stress and local skin warming. We examined the effects of the sGC inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), on reflex skin blood flow responses to whole body heat stress and on nonreflex responses to increased local skin temperature. Blood flow was monitored by laser-Doppler flowmetry, and blood pressure by Finapres to calculate cutaneous vascular conductance (CVC). Intradermal microdialysis was used to treat one site with 1 mM ODQ in 2% DMSO and Ringer, a second site with 2% DMSO in Ringer, and a third site received Ringer. In protocol 1, after a period of normothermia, whole body heat stress was induced. In protocol 2, local heating units warmed local skin temperature from 34 to 41°C to cause local vasodilation. In protocol 1, in normothermia, CVC did not differ among sites [ODQ, 15 ± 3% maximum CVC (CVCmax); DMSO, 14 ± 3% CVCmax; Ringer, 17 ± 6% CVCmax; P > 0.05]. During heat stress, ODQ attenuated CVC increases (ODQ, 54 ± 4% CVCmax; DMSO, 64 ± 4% CVCmax; Ringer, 63 ± 4% CVCmax; P < 0.05, ODQ vs. DMSO or Ringer). In protocol 2, at 34°C local temperature, CVC did not differ among sites (ODQ, 17 ± 2% CVCmax; DMSO, 18 ± 4% CVCmax; Ringer, 18 ± 3% CVCmax; P > 0.05). ODQ attenuated CVC increases at 41°C local temperature (ODQ, 54 ± 5% CVCmax; DMSO, 86 ± 4% CVCmax; Ringer, 90 ± 2% CVCmax; P < 0.05 ODQ vs. DMSO or Ringer). sGC participates in neurogenic active vasodilation during heat stress and in the local response to direct skin warming.

Finger dexterity, skin temperature, and blood flow during auxiliary heating in the cold

2003 ◽  
Vol 95 (2) ◽  
pp. 758-770 ◽  
Author(s):  
Dragan Brajkovic ◽  
Michel B. Ducharme
Keyword(s):  
Blood Flow ◽  
Skin Temperature ◽  
Heat Content ◽  
Finger Dexterity ◽  
Significant Difference ◽  
Forearm Skin ◽  
The Difference ◽  
Finger Skin ◽  
Forearm Muscle ◽  
Body Heat

The primary purpose of the present study was to compare the effectiveness of two forms of hand heating and to discuss specific trends that relate finger dexterity performance to variables such as finger skin temperature (Tfing), finger blood flow (Q̇fing), forearm skin temperature (Tfsk), forearm muscle temperature (Tfmus), mean weighted body skin temperature (T̄sk), and change in body heat content (ΔHb). These variables along with rate of body heat storage, toe skin temperature, and change in rectal temperature were measured during direct and indirect hand heating. Direct hand heating involved the use of electrically heated gloves to keep the fingers warm (heated gloves condition), whereas indirect hand heating involved warming the fingers indirectly by actively heating the torso with an electrically heated vest (heated vest condition). Seven men (age 35.6 ± 5.6 yr) were subjected to each method of hand heating while they sat in a chair for 3 h during exposure to -25°C air. Q̇fing was significantly ( P < 0.05) higher during the heated vest condition compared with the heated gloves condition (234 ± 28 and 33 ± 4 perfusion units, respectively), despite a similar Tfing (which ranged between 28 and 35°C during the 3-h exposure). Despite the difference in Q̇fing, there was no significant difference in finger dexterity performance. Therefore, finger dexterity can be maintained with direct hand heating despite a low Q̇fing. ΔHb, T̄sk, and Tfmus reached a low of -472 ± 18 kJ, 28.5 ± 0.3°C, and 29.8 ± 0.5°C, respectively, during the heated gloves condition, but the values were not low enough to affect finger dexterity.

scholarly journals Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow

2011 ◽  
Vol 111 (3) ◽  
pp. 818-824 ◽  
Author(s):  
Ilkka Heinonen ◽  
R. Matthew Brothers ◽  
Jukka Kemppainen ◽  
Juhani Knuuti ◽  
Kari K. Kalliokoski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Heat Stress ◽  
Local Heating ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Skeletal Muscle Blood Flow ◽  
Whole Body Heat Stress ◽  
Body Heat ◽  
Indirect Heating

For decades it was believed that direct and indirect heating (the latter of which elevates blood and core temperatures without directly heating the area being evaluated) increases skin but not skeletal muscle blood flow. Recent results, however, suggest that passive heating of the leg may increase muscle blood flow. Using the technique of positron-emission tomography, the present study tested the hypothesis that both direct and indirect heating increases muscle blood flow. Calf muscle and skin blood flows were evaluated from eight subjects during normothermic baseline, during local heating of the right calf [only the right calf was exposed to the heating source (water-perfused suit)], and during indirect whole body heat stress in which the left calf was not exposed to the heating source. Local heating increased intramuscular temperature of the right calf from 33.4 ± 1.0°C to 37.4 ± 0.8°C, without changing intestinal temperature. This stimulus increased muscle blood flow from 1.4 ± 0.5 to 2.3 ± 1.2 ml·100 g−1·min−1 ( P < 0.05), whereas skin blood flow under the heating source increased from 0.7 ± 0.3 to 5.5 ± 1.5 ml·100 g−1·min−1 ( P < 0.01). While whole body heat stress increased intestinal temperature by ∼1°C, muscle blood flow in the calf that was not directly exposed to the water-perfused suit (i.e., indirect heating) did not increase during the whole body heat stress (normothermia: 1.6 ± 0.5 ml·100 g−1·min−1; heat stress: 1.7 ± 0.3 ml·100 g−1·min−1; P = 0.87). Whole body heating, however, reflexively increased calf skin blood flow (to 4.0 ± 1.5 ml·100 g−1·min−1) in the area not exposed to the water-perfused suit. These data show that local, but not indirect, heating increases calf skeletal muscle blood flow in humans. These results have important implications toward the reconsideration of previously accepted blood flow distribution during whole body heat stress.

scholarly journals Temperature and blood flow distribution in the human leg during passive heat stress

2016 ◽  
Vol 120 (9) ◽  
pp. 1047-1058 ◽  
Author(s):  
Scott T. Chiesa ◽  
Steven J. Trangmar ◽  
José González-Alonso
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Femoral Vein ◽  
Flow Distribution ◽  
Whole Body ◽  
Temperature Sensitive ◽  
Young Males ◽  
Arterial Blood ◽  
Whole Body Heat Stress ◽  
Body Heat

The influence of temperature on the hemodynamic adjustments to direct passive heat stress within the leg's major arterial and venous vessels and compartments remains unclear. Fifteen healthy young males were tested during exposure to either passive whole body heat stress to levels approaching thermal tolerance [core temperature (Tc) + 2°C; study 1; n = 8] or single leg heat stress (Tc + 0°C; study 2; n = 7). Whole body heat stress increased perfusion and decreased oscillatory shear index in relation to the rise in leg temperature (Tleg) in all three major arteries supplying the leg, plateauing in the common and superficial femoral arteries before reaching severe heat stress levels. Isolated leg heat stress increased arterial blood flows and shear patterns to a level similar to that obtained during moderate core hyperthermia (Tc + 1°C). Despite modest increases in great saphenous venous (GSV) blood flow (0.2 l/min), the deep venous system accounted for the majority of returning flow (common femoral vein 0.7 l/min) during intense to severe levels of heat stress. Rapid cooling of a single leg during severe whole body heat stress resulted in an equivalent blood flow reduction in the major artery supplying the thigh deep tissues only, suggesting central temperature-sensitive mechanisms contribute to skin blood flow alone. These findings further our knowledge of leg hemodynamic responses during direct heat stress and provide evidence of potentially beneficial vascular alterations during isolated limb heat stress that are equivalent to those experienced during exposure to moderate levels of whole body hyperthermia.

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