scholarly journals Mechanisms and modifiers of reflex induced cutaneous vasodilation and vasoconstriction in humans

2010 ◽  
Vol 109 (4) ◽  
pp. 1221-1228 ◽  
Author(s):  
Nisha Charkoudian
Keyword(s):  
Blood Flow ◽  
Human Skin ◽  
Skin Blood Flow ◽  
Cold Exposure ◽  
Heat Dissipation ◽  
Sympathetic Innervation ◽  
Heat Exposure ◽  
Reproductive Hormones ◽  
Excessive Heat ◽  
Cutaneous Vasodilation

Human skin blood flow responses to body heating and cooling are essential to the normal processes of physiological thermoregulation. Large increases in skin blood flow provide the necessary augmentation of convective heat loss during environmental heat exposure and/or exercise, just as reflex cutaneous vasoconstriction is key to preventing excessive heat dissipation during cold exposure. In humans, reflex sympathetic innervation of the cutaneous circulation has two branches: a sympathetic noradrenergic vasoconstrictor system, and a non-noradrenergic active vasodilator system. Noradrenergic vasoconstrictor nerves are tonically active in normothermic environments and increase their activity during cold exposure, releasing both norepinephrine and cotransmitters (including neuropeptide Y) to decrease skin blood flow. The active vasodilator system in human skin does not exhibit resting tone and is only activated during increases in body temperature, such as those brought about by heat exposure or exercise. Active cutaneous vasodilation occurs via cholinergic nerve cotransmission and has been shown to include potential roles for nitric oxide, vasoactive intestinal peptide, prostaglandins, and substance P (and/or neurokinin-1 receptors). It has proven both interesting and challenging that no one substance has been identified as the sole mediator of active cutaneous vasodilation. The processes of reflex cutaneous vasodilation and vasoconstriction are both modified by acute factors, such as exercise and hydration, and more long-term factors, such as aging, reproductive hormones, and disease. This review will highlight some of the recent findings in these areas, as well as interesting areas of ongoing and future work.

scholarly journals Hypoxic cutaneous vasodilation is sustained during brief cold stress and is not affected by changes in CO2

2010 ◽  
Vol 108 (4) ◽  
pp. 788-792 ◽  
Author(s):  
Grant H. Simmons ◽  
Sarah M. Fieger ◽  
Christopher T. Minson ◽  
John R. Halliwill
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Cold Stress ◽  
Skin Blood Flow ◽  
Cold Exposure ◽  
Whole Body ◽  
Cutaneous Vasodilation ◽  
Hypercapnic Hypoxia ◽  
Hypoxic Vasodilation ◽  
The Impact

Hypoxia decreases core body temperature in animals and humans during cold exposure. In addition, hypoxia increases skin blood flow in thermoneutral conditions, but the impact of hypoxic vasodilation on vasoconstriction during cold exposure is unknown. In this study, skin blood flow was assessed using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated as red blood cell flux/mean arterial pressure and normalized to baseline ( n = 7). Subjects were exposed to four different conditions in the steady state (normoxia and poikilocapnic, isocapnic, and hypercapnic hypoxia) and were cooled for 10 min using a water-perfused suit in each condition. CVC increased during all three hypoxic exposures (all P < 0.05 vs. baseline), and the magnitude of these steady-state responses was not affected by changes in end-tidal CO2 levels. During poikilocapnic and hypercapnic hypoxia, cold exposure reduced CVC to the same levels observed during normoxic cooling ( P > 0.05 vs. normoxia), whereas CVC remained elevated throughout cold exposure during isocapnic hypoxia ( P < 0.05 vs. normoxia). The magnitude of vasoconstriction during cold stress was similar in all conditions ( P > 0.05). Thus the magnitude of cutaneous vasodilation during steady-state hypoxia is not affected by CO2 responses. In addition, the magnitude of reflex vasoconstriction is not altered by hypoxia, such that the upward shift in skin blood flow (hypoxic vasodilation) is maintained during whole body cooling.

scholarly journals Effects of mode of exercise recovery on thermoregulatory and cardiovascular responses

2002 ◽  
Vol 93 (6) ◽  
pp. 1918-1924 ◽  
Author(s):  
Robert Carter ◽  
Thad E. Wilson ◽  
Donald E. Watenpaugh ◽  
Michael L. Smith ◽  
Craig G. Crandall
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Heat Dissipation ◽  
Sweat Rate ◽  
Local Heating ◽  
Cardiovascular Responses ◽  
Maximal Heart Rate ◽  
Exercise Recovery ◽  
Active Recovery ◽  
Arterial Blood

To identify the effects of exercise recovery mode on cutaneous vascular conductance (CVC) and sweat rate, eight healthy adults performed two 15-min bouts of upright cycle ergometry at 60% of maximal heart rate followed by either inactive or active (loadless pedaling) recovery. An index of CVC was calculated from the ratio of laser-Doppler flux to mean arterial pressure. CVC was then expressed as a percentage of maximum (%max) as determined from local heating. At 3 min postexercise, CVC was greater during active recovery (chest: 40 ± 3, forearm: 48 ± 3%max) compared with during inactive recovery (chest: 21 ± 2, forearm: 25 ± 4%max); all P < 0.05. Moreover, at the same time point sweat rate was greater during active recovery (chest: 0.47 ± 0.10, forearm: 0.46 ± 0.10 mg · cm−2 · min−1) compared with during inactive recovery (chest: 0.28 ± 0.10, forearm: 0.14 ± 0.20 mg · cm−2 · min−1); all P < 0.05. Mean arterial blood pressure, esophageal temperature, and skin temperature were not different between recovery modes. These data suggest that skin blood flow and sweat rate during recovery from exercise may be modulated by nonthermoregulatory mechanisms and that sustained elevations in skin blood flow and sweat rate during mild active recovery may be important for postexertional heat dissipation.

scholarly journals Aging and the control of human skin blood flow

10.2741/3642 ◽  
2010 ◽  
Vol 15 (1) ◽  
pp. 718 ◽  
Author(s):  
Lacy, A. Holowatz
Keyword(s):  
Blood Flow ◽  
Human Skin ◽  
Skin Blood Flow

Spectral two-wavelength method of quantitative estimation of oxyhemoglobin concentrations in the human-skin blood flow in vivo

1993 ◽  
Author(s):  
Leonid V. Tanin ◽  
Victoria A. Lapina ◽  
Sergei C. Dick ◽  
Serguei A. Alexandrov ◽  
Raisa M. Tanina
Keyword(s):  
Blood Flow ◽  
Human Skin ◽  
Skin Blood Flow ◽  
Quantitative Estimation

scholarly journals Systemic low-dose aspirin and clopidogrel independently attenuate reflex cutaneous vasodilation in middle-aged humans

2010 ◽  
Vol 108 (6) ◽  
pp. 1575-1581 ◽  
Author(s):  
Lacy A. Holowatz ◽  
John D. Jennings ◽  
James A. Lang ◽  
W. Larry Kenney
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Low Dose ◽  
Middle Aged ◽  
Cutaneous Vasodilation ◽  
Dose Aspirin ◽  
Receptor Inhibition ◽  
Low Dose Aspirin ◽  
Adp Receptor ◽  
Reflex Cutaneous Vasodilation

Chronic systemic platelet cyclooxygenase (COX) inhibition with low-dose aspirin [acetylsalicylic acid (ASA)] significantly attenuates reflex cutaneous vasodilation in middle-aged humans, whereas acute, localized, nonisoform-specific inhibition of vascular COX with intradermal administration of ketorolac does not alter skin blood flow during hyperthermia. Taken together, these data suggest that platelets may be involved in reflex cutaneous vasodilation, and this response is inhibited with systemic pharmacological platelet inhibition. We hypothesized that, similar to ASA, specific platelet ADP receptor inhibition with clopidogrel would attenuate reflex vasodilation in middle-aged skin. In a double-blind crossover design, 10 subjects (53 ± 2 yr) were instrumented with four microdialysis fibers for localized drug administration and heated to increase body core temperature [oral temperature (Tor)] 1°C during no systemic drug (ND), and after 7 days of systemic ASA (81 mg) and clopidogrel (75 mg) treatment. Skin blood flow (SkBF) was measured using laser-Doppler flowmetry over each site assigned as 1) control, 2) nitric oxide synthase inhibited (NOS-I; 10 mM NG-nitro-l-arginine methyl ester), 3) COX inhibited (COX-I; 10 mM ketorolac), and 4) NOS-I + COX-I. Data were normalized and presented as a percentage of maximal cutaneous vascular conductance (%CVCmax; 28 mM sodium nitroprusside + local heating to 43°C). During ND conditions, SkBF with change (Δ) in Tor = 1.0°C was 56 ± 3% CVCmax. Systemic low-dose ASA and clopidogrel both attenuated reflex vasodilation (ASA: 43 ± 3; clopidogrel: 32 ± 3% CVCmax; both P < 0.001). In all trials, localized COX-I did not alter SkBF during significant hyperthermia (ND: 56 ± 7; ASA: 43 ± 5; clopidogrel: 35 ± 5% CVCmax; all P > 0.05). NOS-I attenuated vasodilation in ND and ASA (ND: 28 ± 6; ASA: 25 ± 4% CVCmax; both P < 0.001), but not with clopidogrel (27 ± 4% CVCmax; P > 0.05). NOS-I + COX-I was not different compared with NOS-I alone in either systemic treatment condition. Both systemic ASA and clopidogrel reduced the time required to increase Tor 1°C (ND: 58 ± 3 vs. ASA: 45 ± 2; clopidogrel: 39 ± 2 min; both P < 0.001). ASA-induced COX and specific platelet ADP receptor inhibition attenuate reflex vasodilation, suggesting platelet involvement in reflex vasodilation through the release of vasodilating factors.

Regional Variations of Human Skin Blood Flow Response to Histamine

2015 ◽  
pp. 59-66 ◽  
Author(s):  
Ethel Tur ◽  
Galit Aviram ◽  
David Zeltser ◽  
Sarah Brenner ◽  
Howard I. Maibach
Keyword(s):  
Blood Flow ◽  
Human Skin ◽  
Skin Blood Flow ◽  
Regional Variations ◽  
Blood Flow Response ◽  
Flow 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.

scholarly journals Effects of Prior Exercise on Skin Blood Flow and Insulation during Subsequent Moderate Cold Exposure

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Marissa Gayle Spitz ◽  
John W. Castellani ◽  
Martha J Alinovi ◽  
David W DeGroot
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Cold Exposure ◽  
Prior Exercise

Effect of work load on cutaneous vascular response to exercise

1991 ◽  
Vol 71 (4) ◽  
pp. 1614-1619 ◽  
Author(s):  
J. Smolander ◽  
J. Saalo ◽  
O. Korhonen
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Random Order ◽  
Work Load ◽  
Doppler Flowmetry ◽  
Blood Flow Response ◽  
Flow Response ◽  
Cutaneous Vasodilation ◽  
Intensity Of Exercise ◽  
Response To Exercise

The purpose of the present study was to examine whether intensity of exercise affects skin blood flow response to exercise. For this purpose, six healthy men cycled, in a random order on different days, for 15 min at 50, 60, 70, 80, and 90% of their maximum oxygen consumption (VO2max) at a room temperature of 25 degrees C. At the end of exercise, esophageal temperature (Tes) averaged 37.4 +/- 0.2, 37.7 +/- 0.2, 37.9 +/- 0.2, 38.6 +/- 0.3, and 38.9 +/- 0.4 degrees C (SE) at the 50, 60, 70, 80, and 90% work loads, respectively. At the two highest work loads, no steady state was observed in Tes. Skin blood flow was estimated by measuring forearm blood flow (FBF) with strain-gauge plethysmography and by laser-Doppler flowmetry on the upper back. Both techniques showed that skin blood flow response to rising Tes was markedly reduced at the 90% work load compared with other work loads. At the end of exercise, FBF averaged 7.5 +/- 1.7, 10.7 +/- 3.1, 9.6 +/- 2.1, 11.3 +/- 2.6, and 5.4 +/- 1.3 (SE) ml.min-1.100 ml-1 (P less than 0.01) at the 50, 60, 70, 80, and 90% VO2max work loads, respectively. The corresponding values for Tes threshold for cutaneous vasodilation (FBF) were 37.42 +/- 0.16, 37.48 +/- 0.13, 37.59 +/- 0.13, 37.79 +/- 0.19, and 38.20 +/- 0.22 degrees C (P less than 0.05) at 50, 60, 70, 80, and 90% VO2max, respectively. In two subjects, no cutaneous vasodilation was observed at the 90% work load.(ABSTRACT TRUNCATED AT 250 WORDS)

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