The sympathetic release test: a test used to assess thermoregulation and autonomic control of blood flow

2014 ◽  
Vol 38 (1) ◽  
pp. 87-92 ◽  
Author(s):  
E. A. Tansey ◽  
S. M. Roe ◽  
C. D. Johnson

When a subject is heated, the stimulation of temperature-sensitive nerve endings in the skin, and the raising of the central body temperature, results in the reflex release of sympathetic vasoconstrictor tone in the skin of the extremities, causing a measurable temperature increase at the site of release. In the sympathetic release test, the subject is gently heated by placing the feet and calves in a commercially available foot warming pouch or immersing the feet and calves in warm water and wrapping the subject in blankets. Skin blood flow is estimated from measurements of skin temperature in the fingers. Normally skin temperature of the fingers is 65–75°F in cool conditions (environmental temperature: 59–68°F) and rises to 85–95°F during body heating. Deviations in this pattern may mean that there is abnormal sympathetic vasoconstrictor control of skin blood flow. Abnormal skin blood flow can substantially impair an individual's ability to thermoregulate and has important clinical implications. During whole body heating, the skin temperature from three different skin sites is monitored and oral temperature is monitored as an index of core temperature. Students determine the fingertip temperature at which the reflex release of sympathetic activity occurs and its maximal attainment, which reflects the vasodilating capacity of this cutaneous vascular bed. Students should interpret typical sample data for certain clinical conditions (Raynaud's disease, peripheral vascular disease, and postsympathectomy) and explain why there may be altered skin blood flow in these disorders.

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.


2012 ◽  
Vol 18 (7) ◽  
pp. CR415-CR424 ◽  
Author(s):  
Everett B. Lohman III ◽  
Kanikkai Steni Balan Sackiriyas ◽  
Gurinder S. Bains ◽  
Giovanni Calandra ◽  
Crystal Lobo ◽  
...  

2019 ◽  
Vol 84 ◽  
pp. 439-450
Author(s):  
Stephanie Veselá ◽  
Boris R.M. Kingma ◽  
Arjan J.H. Frijns ◽  
Wouter D. van Marken Lichtenbelt

1976 ◽  
Vol 41 (6) ◽  
pp. 826-831 ◽  
Author(s):  
J. M. Johnson ◽  
G. L. Brengelmann ◽  
L. B. Rowell

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.


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.


2012 ◽  
Vol 112 (12) ◽  
pp. 2037-2042 ◽  
Author(s):  
Brett J. Wong ◽  
Sarah M. Fieger

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.


1979 ◽  
Vol 47 (6) ◽  
pp. 1188-1193 ◽  
Author(s):  
J. M. Johnson ◽  
M. K. Park

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.


2019 ◽  
Vol 141 (12) ◽  
Author(s):  
Laura H. Namisnak ◽  
Sepideh Khoshnevis ◽  
Kenneth R. Diller

Abstract The objective of this study was to test the feasibility of selective thermal stimulation (STS) as a method to upregulate glabrous skin blood flow. STS is accomplished by mild surface heating along the spinal cord. Four healthy subjects were tested in this study. Each participated in a control experiment and an intervention experiment (STS). Both experiments included establishing a maximum level of vasodilation, considered unique to a subject on a test day, and then cooling to a maximum level of vasoconstriction. Perfusion was measured by a laser Doppler flow probe on the index fingertip. The percent of perfusion in the range of minimum to maximum was the primary outcome variable. The data were fit to a linear mixed effects model to determine if STS had a significant influence on perfusion during whole body cooling. STS had a statistically significant effect on perfusion and increased glabrous skin blood flow by 16.3% (P < 0.001, CI (13.1%, 19.5%)) as skin temperature was decreased. This study supports the theory that STS improves the heat exchanger efficiency of palmar and plantar surfaces by increasing the blood flow.


2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Jonathan Wingo ◽  
David Low ◽  
David Keller ◽  
Kenichi Kimura ◽  
Scott Davis ◽  
...  

1996 ◽  
Vol 270 (1) ◽  
pp. H208-H215 ◽  
Author(s):  
P. E. Pergola ◽  
J. M. Johnson ◽  
D. L. Kellogg ◽  
W. A. Kosiba

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.


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