scholarly journals Characterizing human skin blood flow regulation in response to different local skin temperature perturbations

2017 ◽  
Vol 111 ◽  
pp. 96-102 ◽  
Author(s):  
Y. Wu ◽  
M.D. Nieuwenhoff ◽  
F.J.P.M. Huygen ◽  
F.C.T. van der Helm ◽  
S. Niehof ◽  
...  
2019 ◽  
Vol 84 ◽  
pp. 439-450
Author(s):  
Stephanie Veselá ◽  
Boris R.M. Kingma ◽  
Arjan J.H. Frijns ◽  
Wouter D. van Marken Lichtenbelt

1988 ◽  
Vol 74 (2) ◽  
pp. 201-206 ◽  
Author(s):  
Ahmad A. K. Hassan ◽  
J. E. Tooke

1. The effects of locally induced alterations in skin temperature on the postural changes in skin blood flow of the foot were assessed in 38 healthy subjects in a constant-temperature environment (22 ± 0.5°C, mean ± sd). 2. Moderate local cooling and warming of the foot (26–36°C) was induced by blowing cold or hot air. Higher ranges of temperature (38–44°C) were achieved by a thermostatically controlled disc heater. 3. Skin blood flow was measured before and during each change in local skin temperature using a laser Doppler flowmeter with the foot maintained at heart level, and placed passively 50 cm below the heart. Blood flow was measured in two skin areas: (i) the dorsum of the foot, where arteriovenous anastomoses are absent, and (ii) the pulp of the big toe, where these anastomoses are relatively numerous. 4. It was found that within the physiological temperature range of 26–36°C the normal postural fall in foot skin blood flow was preserved, whereas it was markedly attenuated or totally abolished at higher temperatures (38–44°C). The pattern of response was quite similar in areas having or lacking arteriovenous anastomoses. 5. It is suggested that the failure of postural vasoconstriction observed at the higher skin temperatures might contribute to some of the problems of cardiovascular adaptations seen in a hot environment.


2015 ◽  
Vol 118 (7) ◽  
pp. 898-903 ◽  
Author(s):  
Gary J. Hodges ◽  
Dean L. Kellogg ◽  
John M. Johnson

The vascular response to local skin cooling is dependent in part on a cold-induced translocation of α2C-receptors and an increased α-adrenoreceptor function. To discover whether β-adrenergic function might contribute, we examined whether β-receptor sensitivity to the β-agonist isoproterenol was affected by local skin temperature. In seven healthy volunteers, skin blood flow was measured from the forearm by laser-Doppler flowmetry and blood pressure was measured by finger photoplethysmography. Data were expressed as cutaneous vascular conductance (CVC; laser-Doppler flux/mean arterial blood pressure). Pharmacological agents were administered via intradermal microdialysis. We prepared four skin sites: one site was maintained at a thermoneutral temperature of 34°C (32 ± 10%CVCmax) one site was heated to 39°C (38 ± 11%CVCmax); and two sites were cooled, one to 29°C (22 ± 7%CVCmax) and the other 24°C (16 ± 4%CVCmax). After 20 min at these temperatures to allow stabilization of skin blood flow, isoproterenol was perfused in concentrations of 10, 30, 100, and 300 μM. Each concentration was perfused for 15 min. Relative to the CVC responses to isoproterenol at the thermoneutral skin temperature (34°C) (+21 ± 10%max), low skin temperatures reduced (at 29°C) (+17 ± 6%max) or abolished (at 24°C) (+1 ± 5%max) the vasodilator response, and warm (39°C) skin temperatures enhanced the vasodilator response (+40 ± 9%max) to isoproterenol. These data indicate that β-adrenergic function was influenced by local skin temperature. This finding raises the possibility that a part of the vasoconstrictor response to direct skin cooling could include reduced background β-receptor mediated vasodilation.


1963 ◽  
Vol 18 (4) ◽  
pp. 781-785 ◽  
Author(s):  
Leo C. Senay ◽  
Leon D. Prokop ◽  
Leslie Cronau ◽  
Alrick B. Hertzman

The relationship of local skin temperature and the onset of sweating to the local cutaneous blood flow was studied in the forearm and calf. The purpose of the investigation was to appraise the possible relation of sweat gland activity to the cutaneous vasodilatation which has been attributed to bradykinin or to intracranial temperatures. The onset of sweating was not marked by any apparently related increases in the rate of cutaneous blood flow. On the contrary, the onset of sweating was followed often by a stabilization or even a decrease in the level of cutaneous blood flow. The relations of the latter to the local skin temperature were complex, particularly in the forearm. There appeared to be additional unidentified influences, possibly vasomotor, operating on the skin vessels during transitional phases in the relation of skin temperature to blood flow. Submitted on October 15, 1962


2005 ◽  
Vol 98 (3) ◽  
pp. 829-837 ◽  
Author(s):  
Yoshi-Ichiro Kamijo ◽  
Kichang Lee ◽  
Gary W. Mack

The role of skin temperature in reflex control of the active cutaneous vasodilator system was examined in six subjects during mild graded heat stress imposed by perfusing water at 34, 36, 38, and 40°C through a tube-lined garment. Skin sympathetic nerve activity (SSNA) was recorded from the peroneal nerve with microneurography. While monitoring esophageal, mean skin, and local skin temperatures, we recorded skin blood flow at bretylium-treated and untreated skin sites by using laser-Doppler velocimetry and local sweat rate by using capacitance hygrometry on the dorsal foot. Cutaneous vascular conductance (CVC) was calculated by dividing skin blood flow by mean arterial pressure. Mild heat stress increased mean skin temperature by 0.2 or 0.3°C every stage, but esophageal and local skin temperature did not change during the first three stages. CVC at the bretylium tosylate-treated site (CVCBT) and sweat expulsion number increased at 38 and 40°C compared with 34°C ( P < 0.05); however, CVC at the untreated site did not change. SSNA increased at 40°C ( P < 0.05, different from 34°C). However, SSNA burst amplitude increased ( P < 0.05), whereas SSNA burst duration decreased ( P < 0.05), at the same time as we observed the increase in CVCBT and sweat expulsion number. These data support the hypothesis that the active vasodilator system is activated by changes in mean skin temperature, even at normal core temperature, and illustrate the intricate competition between active vasodilator and the vasoconstrictor system for control of skin blood flow during mild heat stress.


1994 ◽  
Vol 76 (4) ◽  
pp. 1759-1763 ◽  
Author(s):  
M. V. Savage ◽  
G. L. Brengelmann

Blood flow in human skin increases enormously in response to direct heating. If local skin temperature is held above 42 degrees C, blood flow eventually stabilizes at a level beyond which other influences, barring change in blood pressure, can produce no further increase. If this maximal level is a reproducible characteristic of an individual's cutaneous vasculature, it could be useful in comparing individuals; for example, in their response to hyperthermia. Our experiments were carried out to discover whether the maximal response of the vasculature of the skin of the forearm can be reproduced within reasonable limits and, also, to clarify the time course of the response. We used water sprayed over the surface of the forearms of 10 subjects to hold skin temperature above 42 degrees C for 60 min. During the last 10 min of heating, forearm blood flow (via venous occlusion plethysmography) was stable, at a level ranging from 16 to 38 ml.min-1.100 ml-1. This level, normalized to a blood pressure of 100 mmHg, was reproduced in a given individual on four or five occasions, with an average coefficient of variation of 10%. The response was 77 +/- 11% (SD) complete after 20 min of heating. Elapsed time at 90% of the final value was 35 +/- 9 (SD) min. We conclude that the maximal forearm blood flow response to local heating is a reproducible characteristic of the cutaneous vasculature with potential utility in the scaling of responses between and within individuals.


2006 ◽  
Vol 290 (1) ◽  
pp. R172-R179 ◽  
Author(s):  
Glen P. Kenny ◽  
Jane E. Murrin ◽  
W. Shane Journeay ◽  
Francis D. Reardon

The purpose of this study was to evaluate the possible differences in the postexercise cutaneous vasodilatory response between men and women. Fourteen subjects (7 men and 7 women) of similar age, body composition, and fitness status remained seated resting for 15 min or cycled for 15 min at 70% of peak oxygen consumption followed by 15 min of seated recovery. Subjects then donned a liquid-conditioned suit. Mean skin temperature was clamped at ∼34°C for 15 min. Mean skin temperature was then increased at a rate of 4.3 ± 0.8°C/h while local skin temperature was clamped at 34°C. Skin blood flow was measured continuously at two forearm skin sites, one with (UT) and without (BT) (treated with bretylium tosylate) intact α-adrenergic vasoconstrictor activity. The exercise threshold for cutaneous vasodilation in women (37.51 ± 0.08°C and 37.58 ± 0.04°C for UT and BT, respectively) was greater than that measured in men (37.33 ± 0.06°C and 37.35 ± 0.06°C for UT and BT, respectively) ( P < 0.05). Core temperatures were similar to baseline before the start of whole body warming for all conditions. Postexercise heart rate (HR) for the men (77 ± 4 beats/min) and women (87 ± 6 beats/min) were elevated above baseline (61 ± 3 and 68 ± 4 beats/min for men and women, respectively), whereas mean arterial pressure (MAP) for the men (84 ± 3 mmHg) and women (79 ± 3 mmHg) was reduced from baseline (93 ± 3 and 93 ± 4 mmHg for men and women, respectively) ( P < 0.05). A greater increase in HR and a greater decrease in the MAP postexercise were noted in women ( P < 0.05). No differences in core temperature, HR, and MAP were measured in the no-exercise trial. The postexercise threshold for cutaneous vasodilation measured at the UT and BT sites for men (37.15 ± 0.03°C and 37.16 ± 0.04°C, respectively) and women (37.36 ± 0.05°C and 37.42 ± 0.03°C, respectively) were elevated above no exercise (36.94 ± 0.07°C and 36.97 ± 0.05°C for men and 36.99 ± 0.09°C and 37.03 ± 0.11°C for women for the UT and BT sites, respectively) ( P < 0.05). A difference in the magnitude of the thresholds was measured between women and men ( P < 0.05). We conclude that women have a greater postexercise onset threshold for cutaneous vasodilation than do men and that the primary mechanism influencing the difference between men and women in postexercise skin blood flow is likely the result of an altered active vasodilatory response and not an increase in adrenergic vasoconstrictor tone.


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