scholarly journals Diurnal variation in cutaneous vasodilator and vasoconstrictor systems during heat stress

2001 ◽  
Vol 281 (2) ◽  
pp. R591-R595 ◽  
Author(s):  
Ken Aoki ◽  
Dan P. Stephens ◽  
John M. Johnson
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Diurnal Variation ◽  
Skin Blood Flow ◽  
Whole Body ◽  
Noninvasive Blood Pressure ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Cutaneous Vascular Conductance

It is not clear whether the diurnal variation in the cutaneous circulatory response to heat stress is via the noradrenergic vasoconstrictor system or the nonadrenergic active vasodilator system. We conducted whole body heating experiments in eight male subjects at 0630 (AM) and 1630 (PM). Skin blood flow was monitored by laser-Doppler flowmetry at control sites and at sites pretreated with bretylium (BT) to block noradrenergic vasoconstriction. Noninvasive blood pressure was used to calculate cutaneous vascular conductance. The sublingual temperature (Tor) threshold for cutaneous vasodilation was significantly higher in PM at control and at BT-treated sites (both P < 0.01), suggesting the diurnal shift in threshold depends on the active vasodilator system. The slope of cutaneous vascular conductance as a percentage of its maximum with respect to Tor was significantly lower in AM at control sites only. Also, in the AM, the slope at control sites was significantly lower than that at BT-treated sites ( P < 0.05), suggesting that the diurnal change in the sensitivity of cutaneous vasodilation depends on vasoconstrictor system function. Overall, the diurnal variation in the reflex control of skin blood flow during heat stress involves both vasoconstrictor and active vasodilator systems.

Thermoregulatory reflexes and cutaneous active vasodilation during heat stress in hypertensive humans

1998 ◽  
Vol 85 (1) ◽  
pp. 175-180 ◽  
Author(s):  
D. L. Kellogg ◽  
S. R. Morris ◽  
S. B. Rodriguez ◽  
Y. Liu ◽  
M. Grossmann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Skin Blood Flow ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Forearm Vascular Conductance ◽  
Normotensive Subjects ◽  
Cutaneous Vascular Conductance

During dynamic exercise in the heat, increases in skin blood flow are attenuated in hypertensive subjects when compared with normotensive subjects. We studied responses to passive heat stress (water-perfused suits) in eight hypertensive and eight normotensive subjects. Forearm blood flow was measured by venous-occlusion plethysmography, mean arterial pressure (MAP) was measured by Finapres, and forearm vascular conductance (FVC) was calculated. Bretylium tosylate (BT) iontophoresis was used to block active vasoconstriction in a small area of skin. Skin blood flow was indexed by laser-Doppler flowmetry at BT-treated and untreated sites, and cutaneous vascular conductance was calculated. In normothermia, FVC was lower in hypertensive than in normotensive subjects ( P < 0.01). During heat stress, FVC rose to similar levels in both groups ( P > 0.80); concurrent cutaneous vascular conductance increases were unaffected by BT treatment ( P > 0.60). MAP was greater in hypertensive than in normotensive subjects during normothermia ( P < 0.05, hypertensive vs. normotensive subjects). During hyperthermia, MAP fell in hypertensive subjects but showed no statistically significant change in normotensive subjects ( P < 0.05, hypertensive vs. normotensive subjects). The internal temperature at which vasodilation began did not differ between groups ( P> 0.80). FVC is reduced during normothermia in unmedicated hypertensive subjects; however, they respond to passive heat stress in a fashion no different from normotensive subjects.

Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans

2002 ◽  
Vol 93 (4) ◽  
pp. 1215-1221 ◽  
Author(s):  
D. L. Kellogg ◽  
Y. Liu ◽  
K. McAllister ◽  
C. Friel ◽  
P. E. Pérgola
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Receptor Antagonist ◽  
Healthy Subjects ◽  
Ringer Solution ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Hoe 140 ◽  
Control Body ◽  
Cutaneous Vascular Conductance

To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B2 receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 μM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 ± 2% maximal CVC, P < 0.01) and untreated sites (65 ± 2% maximal CVC, P < 0.01). These responses did not differ between sites ( P > 0.05). Because the bradykinin B2-receptor antagonist HOE-140 did not alter SkBF responses to heat stress, we conclude that bradykinin does not mediate cutaneous active vasodilation.

Effect of increasing central venous pressure during passive heating on skin blood flow

1999 ◽  
Vol 86 (2) ◽  
pp. 605-610 ◽  
Author(s):  
C. G. Crandall ◽  
B. D. Levine ◽  
R. A. Etzel
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Pressure Pulse ◽  
Venous Pressure ◽  
Saline Infusion ◽  
Whole Body ◽  
Passive Heating ◽  
Central Venous ◽  
Vascular Conductance ◽  
Cutaneous Vascular Conductance

Whole body heating in humans increases skin blood flow (SkBF) and decreases central venous pressure (CVP). This study sought to identify whether elevations in SkBF are augmented during passive heating if CVP is increased during the heat stress. Seven subjects were exposed to passive heating. Once SkBF was substantially elevated, 15 ml/kg warm saline were rapidly infused intravenously. Whole body heating significantly increased cutaneous vascular conductance and decreased CVP from 7.7 ± 0.6 to 4.9 ± 0.5 mmHg ( P < 0.05). Saline infusion returned CVP to pre-heat-stress pressures (7.9 ± 0.6 mmHg; P > 0.05) and significantly increased cutaneous vascular conductance relative to the period before saline administration. Moreover, saline infusion did not alter mean arterial pressure, pulse pressure, or esophageal temperature (all P > 0.05). To serve as a volume control, 15 ml/kg saline were rapidly infused intravenously in normothermic subjects. Saline infusion increased CVP ( P < 0.05) without affecting mean arterial pressure, pulse pressure, or cutaneous vascular conductance (all P > 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating may attenuate the elevation in SkBF in humans, whereas loading cardiopulmonary baroreceptors in normothermia has no effect on SkBF.

Cholinergic mechanisms of cutaneous active vasodilation during heat stress in cystic fibrosis

2007 ◽  
Vol 103 (3) ◽  
pp. 963-968 ◽  
Author(s):  
D. L. Kellogg ◽  
G. J. Hodges ◽  
C. R. Orozco ◽  
T. M. Phillips ◽  
J. L. Zhao ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Heat Stress ◽  
Receptor Sensitivity ◽  
Ach Release ◽  
Vascular Conductance ◽  
Cholinergic Mechanisms ◽  
Doppler Flowmetry ◽  
Site Specific ◽  
Cutaneous Vasodilation ◽  
Cutaneous Vascular Conductance

To test the hypothesis that cutaneous active vasodilation in heat stress is mediated by a redundant cholinergic cotransmitter system, we examined the effects of atropine on skin blood flow (SkBF) increases during heat stress in persons with (CF) and without cystic fibrosis (non-CF). Vasoactive intestinal peptide (VIP) has been implicated as a mediator of cutaneous vasodilation in heat stress. VIP-containing cutaneous neurons are sparse in CF, yet SkBF increases during heat stress are normal. In CF, augmented ACh release or muscarinic receptor sensitivity could compensate for decreased VIP; if so, active vasodilation would be attenuated by atropine in CF relative to non-CF. Atropine was administered into skin by iontophoresis in seven CF and seven matched non-CF subjects. SkBF was monitored by laser-Doppler flowmetry (LDF) at atropine treated and untreated sites. Blood pressure [mean arterial pressure (MAP)] was monitored (Finapres), and cutaneous vascular conductance was calculated (CVC = LDF/MAP). The protocol began with a normothermic period followed by a 3-min cold stress and 30–45 min of heat stress. Finally, LDF sites were warmed to 42°C to effect maximal vasodilation. CVC was normalized to its site-specific maximum. During heat stress, CVC increased in both CF and non-CF ( P < 0.01). CVC increases were attenuated by atropine in both groups ( P < 0.01); however, the responses did not differ between groups ( P = 0.99). We conclude that in CF there is not greater dependence on redundant cholinergic mechanisms for cutaneous active vasodilation than in non-CF.

scholarly journals Nitric oxide inhibits cutaneous vasoconstriction to exogenous norepinephrine

2008 ◽  
Vol 105 (5) ◽  
pp. 1504-1508 ◽  
Author(s):  
Manabu Shibasaki ◽  
David A. Low ◽  
Scott L. Davis ◽  
Craig G. Crandall
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Skin Blood Flow ◽  
Whole Body ◽  
Vascular Conductance ◽  
No Donor ◽  
Arterial Blood ◽  
Cutaneous Vascular Conductance ◽  
Cutaneous Vasoconstriction

Previously, we found that nitric oxide (NO) inhibits cutaneous vasoconstrictor responsiveness evoked by whole body cooling, as well as an orthostatic stress in the heat-stressed human (Shibasaki M, Durand S, Davis SL, Cui J, Low DA, Keller DM, Crandall CG. J Physiol 585: 627–634, 2007). However, it remains unknown whether this response occurs via NO acting through presynaptic or postsynaptic mechanisms. The aim of this study was to test the hypothesis that NO is capable of impairing cutaneous vasoconstriction via postsynaptic mechanisms. Skin blood flow was monitored over two forearm sites where intradermal microdialysis membranes were previously placed. Skin blood flow was elevated four- to fivefold through perfusion of the NO donor sodium nitroprusside at one site and through perfusion of adenosine (primarily non-NO mechanisms) at a second site. Once a plateau in vasodilation was evident, increasing concentrations of norepinephrine (1 × 10−8 to 1 × 10−2 M) were administrated through both microdialysis probes, while the aforementioned vasodilator agents continued to be perfused. Cutaneous vascular conductance was calculated by dividing skin blood flow by mean arterial blood pressure. The administration of norepinephrine decreased cutaneous vascular conductance at both sites. However, the dose of norepinephrine at the onset of vasoconstriction (−5.9 ± 1.3 vs. −7.2 ± 0.7 log M norepinephrine, P = 0.021) and the concentration of norepinephrine resulting in 50% of the maximal vasoconstrictor response (−4.9 ± 1.2 vs. −6.1 ± 0.2 log M norepinephrine dose; P = 0.012) occurred at significantly higher norepinephrine concentrations for the sodium nitroprusside site relative to the adenosine site, respectively. These results suggested that NO is capable of attenuating cutaneous vasoconstrictor responsiveness to norepinephrine via postsynaptic mechanisms.

scholarly journals Nonnoradrenergic mechanism of reflex cutaneous vasoconstriction in men

2001 ◽  
Vol 280 (4) ◽  
pp. H1496-H1504 ◽  
Author(s):  
Dan P. Stephens ◽  
Ken Aoki ◽  
Wojciech A. Kosiba ◽  
John M. Johnson
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Adrenergic Receptors ◽  
Whole Body ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Iontophoretic Application ◽  
Β Adrenergic Receptors ◽  
Cutaneous Vascular Conductance ◽  
Cutaneous Vasoconstriction

We tested for a nonnoradrenergic mechanism of reflex cutaneous vasoconstriction with whole body progressive cooling in seven men. Forearm sites (<1 cm2) were pretreated with: 1) yohimbine (Yoh; 5 mM id) to antagonize α-adrenergic receptors, 2) Yoh plus propranolol (5 mM Yoh-1 mM PR id) to block α- and β-adrenergic receptors, 3) iontophoretic application of bretylium tosylate (BT) to block all sympathetic vasoconstrictor nerve effects, or 4) intradermal saline. Skin blood flow was measured by laser Doppler flowmetry and arterial pressure by finger photoplethysmography; cutaneous vascular conductance (CVC) was indexed as the ratio of the two. Whole body skin temperature (TSK) was controlled at 34°C (water-perfused suit) for 10 min and then lowered to 31°C over 15 min. During cooling, vasoconstriction was blocked at BT sites ( P > 0.05). CVC at saline sites fell significantly beginning at TSK of 33.4 ± 0.01°C ( P <0.05). CVC at Yoh-PR sites was significantly reduced beginning at TSK of 33.0 ± 0.01°C ( P < 0.05). After cooling, iontophoretic application of norepinephrine (NE) confirmed blockade of adrenergic receptors by Yoh-PR. Because the effects of NE were blocked at sites showing significant reflex vasoconstriction, a nonnoradrenergic mechanism in human skin is indicated, probably via a sympathetic cotransmitter.

Plasma hyperosmolality elevates the internal temperature threshold for active thermoregulatory vasodilation during heat stress in humans

2009 ◽  
Vol 297 (6) ◽  
pp. R1706-R1712 ◽  
Author(s):  
Manabu Shibasaki ◽  
Ken Aoki ◽  
Keiko Morimoto ◽  
John M. Johnson ◽  
Akira Takamata
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Skin Blood Flow ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Saline Infusion ◽  
Temperature Threshold ◽  
Internal Temperature ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation

Plasma hyperosmolality delays the response in skin blood flow to heat stress by elevating the internal temperature threshold for cutaneous vasodilation. This elevation could be because of a delayed onset of cutaneous active vasodilation and/or to persistent cutaneous active vasoconstriction. Seven healthy men were infused with either hypertonic (3% NaCl) or isotonic (0.9% NaCl) saline and passively heated by immersing their lower legs in 42°C water for 60 min (room temperature, 28°C; relative humidity, 40%). Skin blood flow was monitored via laser-Doppler flowmetry at sites pretreated with bretylium tosylate (BT) to block sympathetic vasoconstriction selectively and at adjacent control sites. Plasma osmolality was increased by ∼13 mosmol/kgH2O following hypertonic saline infusion and was unchanged following isotonic saline infusion. The esophageal temperature (Tes) threshold for cutaneous vasodilation at untreated sites was significantly elevated in the hyperosmotic state (37.73 ± 0.11°C) relative to the isosmotic state (36.63 ± 0.12°C, P < 0.001). A similar elevation of the Tes threshold for cutaneous vasodilation was observed between osmotic conditions at the BT-treated sites (37.74 ± 0.18 vs. 36.67 ± 0.07°C, P < 0.001) as well as sweating. These results suggest that the hyperosmotically induced elevation of the internal temperature threshold for cutaneous vasodilation is due primarily to an elevation in the internal temperature threshold for the onset of active vasodilation, and not to an enhancement of vasoconstrictor activity.

scholarly journals Methodological assessment of skin and limb blood flows in the human forearm during thermal and baroreceptor provocations

2010 ◽  
Vol 109 (3) ◽  
pp. 895-900 ◽  
Author(s):  
R. Matthew Brothers ◽  
Jonathan E. Wingo ◽  
Kimberly A. Hubing ◽  
Craig G. Crandall
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Doppler Ultrasound ◽  
Skin Blood Flow ◽  
Skin Surface ◽  
Laser Doppler ◽  
Whole Body ◽  
Surface Cooling ◽  
Doppler Flowmetry ◽  
Human Forearm

Skin blood flow responses in the human forearm, assessed by three commonly used technologies—single-point laser-Doppler flowmetry, integrated laser-Doppler flowmetry, and laser-Doppler imaging—were compared in eight subjects during normothermic baseline, acute skin-surface cooling, and whole body heat stress (Δ internal temperature = 1.0 ± 0.2°C; P < 0.001). In addition, while normothermic and heat stressed, subjects were exposed to 30-mmHg lower-body negative pressure (LBNP). Skin blood flow was normalized to the maximum value obtained at each site during local heating to 42°C for at least 30 min. Furthermore, comparisons of forearm blood flow (FBF) measures obtained using venous occlusion plethysmography and Doppler ultrasound were made during the aforementioned perturbations. Relative to normothermic baseline, skin blood flow decreased during normothermia + LBNP ( P < 0.05) and skin-surface cooling ( P < 0.01) and increased during whole body heating ( P < 0.001). Subsequent LBNP during whole body heating significantly decreased skin blood flow relative to control heat stress ( P < 0.05). Importantly, for each of the aforementioned conditions, skin blood flow was similar between the three measurement devices (main effect of device: P > 0.05 for all conditions). Similarly, no differences were identified across all perturbations between FBF measures using plethysmography and Doppler ultrasound ( P > 0.05 for all perturbations). These data indicate that when normalized to maximum, assessment of skin blood flow in response to vasoconstrictor and dilator perturbations are similar regardless of methodology. Likewise, FBF responses to these perturbations are similar between two commonly used methodologies of limb blood flow assessment.

Cutaneous interstitial nitric oxide concentration does not increase during heat stress in humans

2001 ◽  
Vol 90 (3) ◽  
pp. 1020-1024 ◽  
Author(s):  
C. G. Crandall ◽  
D. A. MacLean
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Heat Stress ◽  
Skin Blood Flow ◽  
Whole Body ◽  
Cutaneous Vasodilation ◽  
Oxide Concentration ◽  
Forearm Skin ◽  
Nitric Oxide Concentration ◽  
Permissive Role

Inhibition of cutaneous nitric oxide (NO) synthase reduces the magnitude of cutaneous vasodilation during whole body heating in humans. However, this observation is insufficient to conclude that NO concentration increases in the skin during a heat stress. This study was designed to test the hypothesis that whole body heating increases cutaneous interstitial NO concentration. This was accomplished by placing 2 microdialysis membranes in the forearm dermal space of 12 subjects. Both membranes were perfused with lactated Ringer solutions at a rate of 2 μl/min. In both normothermia and during whole body heating via a water perfused suit, dialysate from these membranes were obtained and analyzed for NO using the chemiluminescence technique. In six of these subjects, after the heat stress, the membranes were perfused with a 1 M solution of acetylcholine to stimulate NO release. Dialysate from these trials was also assayed to quantify cutaneous interstitial NO concentration. Whole body heating increased skin temperature from 34.6 ± 0.2 to 38.8 ± 0.2°C ( P < 0.05), which increased sublingual temperature (36.4 ± 0.1 to 37.6 ± 0.1°C; P < 0.05), heart rate (63 ± 5 to 93 ± 5 beats/min; P < 0.05), and skin blood flow over the membranes (21 ± 4 to 88 ± 10 perfusion units; P < 0.05). NO concentration in the dialysate did not increase significantly during of the heat stress (7.6 ± 0.7 to 8.6 ± 0.8 μM; P > 0.05). After the heat stress, administration of acetylcholine in the perfusate significantly increased skin blood flow (128 ± 6 perfusion units) relative to both normothermic and heat stress values and significantly increased NO concentration in the dialysate (15.8 ± 2.4 μM). These data suggest that whole body heating does not increase cutaneous interstitial NO concentration in forearm skin. Rather, NO may serve in a permissive role in facilitating the effects of an unknown neurotransmitter, leading to cutaneous vasodilation during a heat stress.

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.

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