Reflex control of active cutaneous vasodilation by skin temperature in humans

1994 ◽  
Vol 266 (5) ◽  
pp. H1979-H1984 ◽  
Author(s):  
P. E. Pergola ◽  
D. L. Kellogg ◽  
J. M. Johnson ◽  
W. A. Kosiba
Keyword(s):  
Blood Flow ◽  
Skin Temperature ◽  
Control Site ◽  
Whole Body ◽  
Entire Body ◽  
Internal Temperature ◽  
Doppler Flowmetry ◽  
Vasodilator Activity ◽  
Forearm Skin ◽  
Reflex Control

The purpose of this study was to examine whether reflex effects of changes in whole body skin temperature (Tsk) on cutaneous vasculature are mediated through the vasoconstrictor or the active vasodilator arm of the sympathetic nervous system. In six subjects, reflex responses in forearm skin blood flow (SkBF) to changes in Tsk were monitored by laser-Doppler flowmetry. SkBF was monitored at a control site and at a 0.6-cm2 site where bretylium (BT) had been iontophoretically applied to abolish sympathetic vasoconstrictor control. Reflex control of SkBF at BT-treated sites is solely through active vasodilator activity. An index of cutaneous vascular conductance (CVC) was calculated from the blood flow signal and mean arterial pressure, measured noninvasively. Data are expressed relative to maximum CVC (CVCmax) achieved by local warming of measurement sites to 42 degrees C at the end of each study. Tsk was controlled with a water-perfused suit covering the entire body except for the head and arms. Esophageal temperature (Tes) was measured as an index of internal temperature. In part A (rest), raising Tsk at rest from 31.9 +/- 0.3 to 36.7 +/- 0.2 degrees C increased CVC at control sites from 3 +/- 0.2 to 5 +/- 0.6% of CVCmax. CVC did not change at BT-treated sites, suggesting that at rest, with a normal internal temperature, reflex effects of raising Tsk on SkBF are mediated through vasoconstrictor withdrawal. In part B (exercise), exercise at a low Tsk increased Tes to 37.49 +/- 0.1 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

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)

Reflex control of skin blood flow by skin temperature: role of core temperature

1979 ◽  
Vol 47 (6) ◽  
pp. 1188-1193 ◽  
Author(s):  
J. M. Johnson ◽  
M. K. Park
Keyword(s):  
Blood Flow ◽  
Skin Temperature ◽  
Skin Blood Flow ◽  
Work Load ◽  
Reflex Response ◽  
Esophageal Temperature ◽  
Internal Temperature ◽  
Reflex Control ◽  
Different Levels

Two protocols were used to discover whether the reflex response in skin blood flow (SkBF) to rising skin temperature (Tsk) was dependent on the level of internal temperature. Part I. In five subjects, Tsk (controlled with water-perfused suits) was raised to 37 degrees C prior to, between 2 and 5 min, or between 10 and 17 min of exercise. The associated SkBF elevation per degree rise in Tsk averaged 0.20, 1.28, and 1.75 ml/100 ml . min, respectively. When Tsk was raised during the first 5 min of exercise, esophageal temperature (Tes) rose markedly (0.39 degrees C), but transiently fell if Tsk was raised after 10 min of exercise. Part II. In six subjects, different work loads were used to develop different levels of internal temperature. Tsk was elevated to 37 degrees C after 10--15 min at light (50--75 W) or moderate (100--150 W) work loads. At the heavier work load (and higher Tes), the rise in forearm SkBF per degree rise in Tsk averaged 2.33 +/- 0.38 (SE) times that observed at the light work load. These data strongly suggest that the reflex response of SkBF to rising Tsk is dependent on the level of internal temperature.

Control of skin blood flow by whole body and local skin cooling in exercising humans

1996 ◽  
Vol 270 (1) ◽  
pp. H208-H215 ◽  
Author(s):  
P. E. Pergola ◽  
J. M. Johnson ◽  
D. L. Kellogg ◽  
W. A. Kosiba
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Threshold Level ◽  
Tissue Temperature ◽  
Whole Body ◽  
Internal Temperature ◽  
Local Cooling ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Rate Of Increase

We examined the independent roles of whole body skin temperature (Tsk) and tissue temperature (local temperature, Tloc) in the control of skin blood flow (SBF) during cooling and the roles of the vasoconstrictor (VC) and active vasodilator (AVD) systems in mediating these effects. SBF was monitored by laser-Doppler flowmetry (LDF) at untreated sites and sites with local VC blockade by pretreatment with bretylium (BT). Seven subjects underwent four sessions of moderate bicycle exercise (20-30 min duration) at neutral Tsk and Tloc (34 degrees C), neutral Tsk and cool Tloc (27 degrees C), low Tsk (28 degrees C) and neutral Tloc, and low Tsk and Tloc. Cutaneous vascular conductance (CVC; LDF/mean arterial pressure) was expressed relative to the maximum. Cool Tsk increased the threshold level of internal temperature at which CVC began to rise equally at BT-treated and untreated sites (P < 0.05). The rate of increase in CVC relative to internal temperature was reduced by local cooling. BT pretreatment partially reversed this effect (P < 0.05). Thus a cool environment results in reflex inhibition of the onset of AVD activity by cool Tsk and a reduced rate of increase in CVC due, in part, to norepinephrine release stimulated by cool Tloc.

Forearm blood flow during body temperature transients produced by leg exercise

1975 ◽  
Vol 38 (1) ◽  
pp. 58-63 ◽  
Author(s):  
C. B. Wenger ◽  
M. F. Roberts ◽  
J. A. Stolwijk ◽  
E. R. Nadel
Keyword(s):  
Blood Flow ◽  
Skin Temperature ◽  
Forearm Blood Flow ◽  
Bicycle Ergometer ◽  
Vapor Pressures ◽  
Internal Temperature ◽  
Ambient Temperatures ◽  
Forearm Skin ◽  
Leg Exercise ◽  
Skin Temperatures

Subjects exercised for 30 min on a bicycle ergometer at 30, 50, and 70% of maximal aerobic power in ambient temperatures of 15, 25, and 35 degrees C and vapor pressures of less than 18 Torr. Exercise was used to vary internal temperature during an experiment, and different ambient temperatures were used to vary skin temperatures independently of internal temperature. Forearm skin temperature was fixed at about 36.5 degrees C. Esophageal temperature (Tes) was measured with a thermocouple at the level of the left atrium, and mean skin temperature (Tsk) was calculated from a weighted mean of thermocouple temperatures at eight skin sites. Forearm blood flow (BF) was measured by electrocapacitance plethysmography. Our data are well accounted for by an equation of the form BF = a1Tes + q2Tsk + b, independent of exercise intensity, although some subjects showed an equivocal vasodilator effect of exercise. The ratios a1/a2 (7.5, 9.6, 11.7) are quite similar to the ratios (8.6, 10.4) of the corresponding coefficients in two recent models of thermoregulatory sweating.

Prostanoids contribute to cutaneous active vasodilation in humans

2006 ◽  
Vol 291 (3) ◽  
pp. R596-R602 ◽  
Author(s):  
Gregg R. McCord ◽  
Jean-Luc Cracowski ◽  
Christopher T. Minson
Keyword(s):  
Core Body Temperature ◽  
Local Heating ◽  
Ringer Solution ◽  
Control Site ◽  
Whole Body ◽  
Nitric Oxide Synthase Inhibitor ◽  
Doppler Flowmetry ◽  
Forearm Skin ◽  
Synthase Inhibitor ◽  
Hyperemic Response

The specific mechanisms by which skin blood flow increases in response to a rise in core body temperature via cutaneous active vasodilation are poorly understood. The primary purpose of this study was to determine whether the cyclooxygenase (COX) pathway contributes to active vasodilation during whole body heat stress ( protocol 1; n = 9). A secondary goal was to verify that the COX pathway does not contribute to the cutaneous hyperemic response during local heating ( protocol 2; n = 4). For both protocols, four microdialysis fibers were placed in forearm skin. Sites were randomly assigned and perfused with 1) Ringer solution (control site); 2) ketorolac (KETO), a COX-1/COX-2 pathway inhibitor; 3) NG-nitro-l-arginine methyl ester (l-NAME), a nitric oxide synthase inhibitor; and 4) a combination of KETO and l-NAME. During the first protocol, active vasodilation was induced using whole body heating with water-perfused suits. The second protocol used local heaters to induce a local hyperemic response. Red blood cell flux (RBC flux) was indexed at all sites using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC; RBC flux/mean arterial pressure) was normalized to maximal vasodilation at each site. During whole body heating, CVC values at sites perfused with KETO (43 ± 9% CVCmax), l-NAME (35 ± 9% CVCmax), and combined KETO/l-NAME (22 ± 8% CVCmax) were significantly decreased with respect to the control site (59 ± 7% CVCmax) ( P < 0.05). Additionally, CVC at the combined KETO/l-NAME site was significantly decreased compared with sites infused with KETO or l-NAME alone ( P < 0.05). In the second protocol, the hyperemic response to local heating did not differ between the control site and KETO site or between the l-NAME and KETO/l-NAME site. These data suggest that prostanoids contribute to active vasodilation, but do not play a role during local thermal hyperemia.

Role of sympathetic nerves in the vascular effects of local temperature in human forearm skin

1993 ◽  
Vol 265 (3) ◽  
pp. H785-H792 ◽  
Author(s):  
P. E. Pergola ◽  
D. L. Kellogg ◽  
J. M. Johnson ◽  
W. A. Kosiba ◽  
D. E. Solomon
Keyword(s):  
Skin Temperature ◽  
Whole Body ◽  
Adrenergic Nerve ◽  
Local Cooling ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Human Forearm ◽  
Forearm Skin ◽  
Local Warming

The role of adrenergic nerve function in the cutaneous vascular response to changes in local skin temperature in the human forearm was examined using three protocols: 1) blocking release of norepinephrine presynaptically by local iontophoresis of bretylium (BT), 2) altering background adrenergic tone by changing whole body skin temperature, and 3) blocking cutaneous nerves by proximal infiltration of local anesthetic. Forearm skin blood flow was measured by laser-Doppler flowmetry (LDF) and cutaneous vascular conductance (CVC) was calculated as LDF/blood pressure. In protocol 1, local cooling (29 degrees C) elicited a rapid and sustained fall in CVC at control sites (-43 +/- 8%) in contrast to a biphasic response at BT-treated sites, consisting of an initial vasodilation followed by a vasoconstriction (percent change CVC = 28 +/- 13 and -34 +/- 18, respectively). Local warming (39 degrees C) increased CVC at control and at BT-treated sites by 331 +/- 46 and 139 +/- 31%, respectively. In protocol 2, at a neutral, cool, or warm whole body skin temperature, local cooling (29 degrees C) elicited similar reductions in CVC (-34 +/- 8, -29 +/- 5, and -30 +/- 4%, respectively), and local warming (38 degrees C) produced similar increases in CVC (89 +/- 15, 85 +/- 21, and 74 +/- 22%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Ketorolac alters blood flow during normothermia but not during hyperthermia in middle-aged human skin

2009 ◽  
Vol 107 (4) ◽  
pp. 1121-1127 ◽  
Author(s):  
Lacy A. Holowatz ◽  
John D. Jennings ◽  
James A. Lang ◽  
W. Larry Kenney
Keyword(s):  
Blood Flow ◽  
Human Skin ◽  
Control Site ◽  
Middle Aged ◽  
Doppler Flowmetry ◽  
Healthy Humans ◽  
Cutaneous Vasodilation ◽  
Forearm Skin ◽  
Oxide Synthase ◽  
Reflex Cutaneous Vasodilation

In young healthy humans full expression of reflex cutaneous vasodilation is dependent on cyclooxygenase (COX)- and nitric oxide synthase (NOS)-dependent mechanisms. Chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilation potentially through both platelet and vascular COX-dependent mechanisms. We hypothesized the contribution of COX-dependent vasodilators to reflex cutaneous vasodilation during localized acute COX inhibition would be attenuated in healthy middle-aged humans due to a shift toward COX-dependent vasoconstrictors. Four microdialysis fibers were placed in forearm skin of 13 middle-aged (53 ± 2 yr) normotensive healthy humans, serving as control (Ringer), COX-inhibited (10 mM ketorolac), NOS-inhibited (10 mM NG-nitro-l-arginine methyl ester), and combined NOS- and COX-inhibited sites. Red blood cell flux was measured over each site by laser-Doppler flowmetry as reflex vasodilation was induced by increasing oral temperature (Tor) 1.0°C using a water-perfused suit. Cutaneous vascular conductance was calculated (CVC = flux/mean arterial pressure) and normalized to maximal CVC (CVCmax; 28 mM sodium nitroprusside). CVCmax was not affected by localized microdialysis drug treatment ( P > 0.05). Localized COX inhibition increased baseline (18 ± 3%CVCmax; P < 0.001) compared with control (9 ± 1%CVCmax), NOS-inhibited (7 ± 1%CVCmax), and combined sites (10 ± 1%CVCmax). %CVCmax in the COX-inhibited site remained greater than the control site with ΔTor ≤ 0.3°C; however, there was no difference between these sites with ΔTor ≥ 0.4°C. NOS inhibition and combined COX and NOS inhibition attenuated reflex vasodilation compared with control ( P < 0.001), but there was no difference between these sites. Localized COX inhibition with ketorolac significantly augments baseline CVC but does not alter the subsequent skin blood flow response to hyperthermia, suggesting a limited role for COX-derived vasodilator prostanoids in reflex cutaneous vasodilation and a shift toward COX-derived vasoconstrictors in middle-aged human skin.

scholarly journals Minimal role for H1 and H2 histamine receptors in cutaneous thermal hyperemia to local heating in humans

2006 ◽  
Vol 100 (2) ◽  
pp. 535-540 ◽  
Author(s):  
Brett J. Wong ◽  
Sarah J. Williams ◽  
Christopher T. Minson
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Histamine Receptor ◽  
Receptor Activation ◽  
Control Site ◽  
Doppler Flowmetry ◽  
Histamine Receptor Antagonist ◽  
And Control

The precise mechanism(s) underlying the thermal hyperemic response to local heating of human skin are not fully understood. The purpose of this study was to investigate a potential role for H1 and H2 histamine-receptor activation in this response. Two groups of six subjects participated in two separate protocols and were instrumented with three microdialysis fibers on the ventral forearm. In both protocols, sites were randomly assigned to receive one of three treatments. In protocol 1, sites received 1) 500 μM pyrilamine maleate (H1-receptor antagonist), 2) 10 mM l-NAME to inhibit nitric oxide synthase, and 3) 500 μM pyrilamine with 10 mM NG-nitro-l-arginine methyl ester (l-NAME). In protocol 2, sites received 1) 2 mM cimetidine (H2 antagonist), 2) 10 mM l-NAME, and 3) 2 mM cimetidine with 10 mM l-NAME. A fourth site served as a control site (no microdialysis fiber). Skin sites were locally heated from a baseline of 33 to 42°C at a rate of 0.5°C/5 s, and skin blood flow was monitored using laser-Doppler flowmetry (LDF). Cutaneous vascular conductance was calculated as LDF/mean arterial pressure. To normalize skin blood flow to maximal vasodilation, microdialysis sites were perfused with 28 mM sodium nitroprusside, and control sites were heated to 43°C. In both H1 and H2 antagonist studies, no differences in initial peak or secondary plateau phase were observed between control and histamine-receptor antagonist only sites or between l-NAME and l-NAME with histamine receptor antagonist. There were no differences in nadir response between l-NAME and l-NAME with histamine-receptor antagonist. However, the nadir response in H1 antagonist sites was significantly reduced compared with control sites, but there was no effect of H2 antagonist on the nadir response. These data suggest only a modest role for H1-receptor activation in the cutaneous response to local heating as evidenced by a diminished nadir response and no role for H2-receptor activation.

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.

Reflex regulation of sweat rate by skin temperature in exercising humans

1984 ◽  
Vol 56 (5) ◽  
pp. 1283-1288 ◽  
Author(s):  
J. M. Johnson ◽  
D. S. O'Leary ◽  
W. F. Taylor ◽  
M. K. Park
Keyword(s):  
Blood Flow ◽  
Regression Analysis ◽  
Linear Regression ◽  
Skin Temperature ◽  
Sweat Rate ◽  
Linear Regression Analysis ◽  
Multiple Linear Regression Analysis ◽  
Esophageal Temperature ◽  
Reflex Regulation ◽  
Forearm Skin

To find whether sweat rate (SR) and forearm skin blood flow ( SkBF ) were reflexly affected by skin temperature (Tsk) we used water-perfused suits to rapidly elevate Tsk during exercise. With this elevation in Tsk, there was a period of little net change in esophageal temperature (Tes) but marked responses in SR and SkBF . During this period a rise in Tsk of 4.2 +/- 0.3 degrees C was associated with an increase in SR of 0.44 +/- 0.09 mg X cm-2 X min-1 and an increase in SkBF of 3.27 +/- 0.42 ml X 100 ml-1 X min-1. Multiple linear regression analysis as well as comparison with control studies in which Tsk was kept cool also reveal a consistent role for Tsk in the reflex regulation of SR and SkBF . Responses in SR and FBF were much more marked at levels of Tsk below 33 degrees C. Below a Tsk of 33 degrees C, SR rose 0.30 +/- 0.06 mg X cm-2 X min-1 per degrees C rise in Tsk, whereas above 33 degrees SR rose only 0.05 +/- 0.01 mg X cm2 X min per degrees C. FBF rose 2.81 +/- 0.60 and 0.77 +/- 0.18 ml X 100 ml-1 X min-1 per degrees C rise in Tsk at the lower and upper ranges of Tsk, respectively.

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