Modification of cutaneous vasodilator response to heat stress by daytime exogenous melatonin administration

2006 ◽  
Vol 291 (3) ◽  
pp. R619-R624 ◽  
Author(s):  
Ken Aoki ◽  
Dan P. Stephens ◽  
Kun Zhao ◽  
Wojciech A. Kosiba ◽  
John M. Johnson
Keyword(s):  
Heat Stress ◽  
Random Order ◽  
Vascular Conductance ◽  
Exogenous Melatonin ◽  
Shift Control ◽  
Melatonin Administration ◽  
Relationship Of ◽  
The Relationship ◽  
Cutaneous Vascular Conductance ◽  
Male Subjects

In humans, the nocturnal fall in internal temperature is associated with increased endogenous melatonin and with a shift in the thermoregulatory control of skin blood flow (SkBF), suggesting a role for melatonin in the control of SkBF. The purpose of this study was to test whether daytime exogenous melatonin would shift control of SkBF to lower internal temperatures during heat stress, as is seen at night. Healthy male subjects ( n = 8) underwent body heating with melatonin administration (Mel) or without (control), in random order at least 1 wk apart. SkBF was monitored at sites pretreated with bretylium to block vasoconstrictor nerve function and at untreated sites. Cutaneous vascular conductance, calculated from SkBF and arterial pressure, sweating rate (SR), and heart rate (HR) were monitored. Skin temperature was elevated to 38°C for 35–50 min. Baseline esophageal temperature (Tes) was lower in Mel than in control ( P < 0.01). The Tes threshold for cutaneous vasodilation and the slope of cutaneous vascular conductance with respect to Tes were also lower in Mel at both untreated and bretylium-treated sites ( P < 0.05). The Tes threshold for the onset of sweating and the Tes for a standard HR were reduced in Mel. The slope of the relationship of HR, but not SR, to Tes was lower in Mel ( P < 0.05). These findings suggest that melatonin affects the thermoregulatory control of SkBF during hyperthermia via the cutaneous active vasodilator system. Because control of SR and HR are also modified, a central action of melatonin is suggested.

scholarly journals Small reductions in skin temperature after onset of a simulated hemorrhagic challenge improve tolerance in exercise heat-stressed individuals

2018 ◽  
Vol 315 (3) ◽  
pp. R539-R546
Author(s):  
Claire E. Trotter ◽  
Faith K. Pizzey ◽  
Philip M. Batterson ◽  
Robert A. Jacobs ◽  
James Pearson
Keyword(s):  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Skin Temperature ◽  
Healthy Subjects ◽  
Lower Body Negative Pressure ◽  
Stress Index ◽  
Lower Body ◽  
Vascular Conductance ◽  
Cumulative Stress ◽  
Cutaneous Vascular Conductance

We investigated whether small reductions in skin temperature 60 s after the onset of a simulated hemorrhagic challenge would improve tolerance to lower body negative pressure (LBNP) after exercise heat stress. Eleven healthy subjects completed two trials (High and Reduced). Subjects cycled at ~55% maximal oxygen uptake wearing a warm water-perfused suit until core temperatures increased by ~1.2°C before lying supine and undergoing LBNP to presyncope. LBNP tolerance was quantified as cumulative stress index (CSI; product of each LBNP level multiplied by time; mmHg·min). Skin temperature was similarly elevated from baseline before LBNP and remained elevated 60 s after the onset of LBNP in both High (37.72 ± 0.52°C) and Reduced (37.95 ± 0.54°C) trials (both P < 0.0001). At 60%CSI skin temperature remained elevated in the High trial (37.51 ± 0.56°C) but was reduced to 34.97 ± 0.72°C by the water-perfused suit in the Reduced trial ( P < 0.0001 between trials). Cutaneous vascular conductance was not different between trials [High: 1.57 ± 0.43 vs. Reduced: 1.39 ± 0.38 arbitrary units (AU)/mmHg; P = 0.367] before LBNP but decreased to 0.67 ± 0.19 AU/mmHg at 60%CSI in the Reduced trial while remaining unchanged in the High trial ( P = 0.002 between trials). CSI was higher in the Reduced (695 ± 386 mmHg·min) relative to the High (441 ± 290 mmHg·min; P = 0.023) trial. Mean arterial pressure was not different between trials at presyncope (High: 62 ± 10 vs. Reduced: 62 ± 9 mmHg; P = 0.958). Small reductions in skin temperature after the onset of a simulated hemorrhagic challenge improve LBNP tolerance after exercise heat stress. This may have important implications regarding treatment of an exercise heat-stressed individual (e.g., soldier) who has experienced a hemorrhagic injury.

Role of glutathione on recovery of red-osier dogwood plants from "near-lethal" heat stress

1994 ◽  
Vol 24 (2) ◽  
pp. 415-418 ◽  
Author(s):  
A.M. Shirazi ◽  
J.H. Siller-Cepeda ◽  
L.H. Fuchigami
Keyword(s):  
Heat Stress ◽  
Stress Environment ◽  
Relationship Of ◽  
The Relationship ◽  
Post Stress

This study reports on the relationship of glutathione to the recovery and death of red-osier dogwood, Cornussericea L., plants from "near-lethal" (NL) heat stress. Shoots of dormant red-osier dogwood plants were exposed to 51 °C for 1 h during early February, and then incubated in the dark at either 0 or 23 °C post-stress environment (PSE). In a previous study, NL heat stress treated plants incubated at 23 and 0 °C PSE recovered and died, respectively. Reduced and oxidized forms of glutathione (GSH and GSSG, respectively) were measured with HPLC at 365 nm absorbance after 0 h, 24 h, 2 weeks, and 4 weeks PSE, respectively. Incubation of the NL heat stress treatments for 24 h at 23 ± 3 °C prior to post-treatments resulted in a significant decrease of GSSG and slight decrease of GSH. In contrast, the sudden exposure of NL stressed plants to 0 °C for 24 h resulted in a significant reduction of both GSH and GSSG levels after 2 and 4 weeks incubation. At 23 °C PSE, GSH and GSSG levels of NL heat stressed plants increased, while at 0 °C PSE the levels of both decreased.

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.

scholarly journals Continuous measurement of tympanic temperature with a new infrared method using an optical fiber

1998 ◽  
Vol 85 (3) ◽  
pp. 921-926 ◽  
Author(s):  
Manabu Shibasaki ◽  
Narihiko Kondo ◽  
Hirotaka Tominaga ◽  
Ken Aoki ◽  
Eiichi Hasegawa ◽  
...  
Keyword(s):  
Optical Fiber ◽  
Tympanic Temperature ◽  
Temperature Threshold ◽  
Exercise Tests ◽  
Head Cooling ◽  
Significant Difference ◽  
Infrared Method ◽  
Relationship Of ◽  
The Relationship ◽  
Male Subjects

The purpose of this study was to investigate the utility of an infrared tympanic thermometry by using an optical fiber for measuring tympanic temperature (Tty). In the head cooling and facial fanning tests during normothermia, right Tty measured by this method (infrared-Tty) and esophageal temperature (Tes) were not affected by decreased temple and forehead skin temperatures, suggesting that the infrared sensor in this system measured the infrared radiation from the tympanic membrane selectively. Eight male subjects took part in passive-heat-stress and progressive-exercise tests. No significant differences among infrared-Tty, the left Tty measured by thermistor (contact-Tty), and Tes were observed at rest or at the end of each experiment, and there was no significant difference in the increase in these core temperatures from rest to the end. Furthermore, there were no significant differences in the core temperature threshold at the onset of sweating and slope (the relationship of sweating rate vs. infrared-Tty and vs. contact-Tty). These results suggest that this method makes it possible to measure Tty accurately, continuously, and more safely.

Reflex control of cutaneous vasoconstrictor system is reset by exogenous female reproductive hormones

1999 ◽  
Vol 87 (1) ◽  
pp. 381-385 ◽  
Author(s):  
Nisha Charkoudian ◽  
John M. Johnson
Keyword(s):  
Contraceptive Use ◽  
Reproductive Hormones ◽  
Doppler Flowmetry ◽  
Oral Contraceptive Use ◽  
Vasoconstrictor Response ◽  
Reflex Control ◽  
Relationship Of ◽  
The Relationship ◽  
Cutaneous Vascular Conductance ◽  
Cutaneous Vasoconstriction

To determine whether cardiovascular influences of exogenous female steroid hormones include effects on reflex thermoregulatory control of the adrenergic cutaneous vasoconstrictor system, we conducted ramp decreases in skin temperature (Tsk) in eight women in both high- and low (placebo)-progesterone/estrogen phases of oral contraceptive use. With the use of water-perfused suits, Tsk was held at 36°C for 10 min (to minimize initial vasoconstrictor activity) and was then decreased in a ramp, ∼0.2°C/min for 12–15 min. Subjects rested supine for 30–40 min before each experiment, and the protocol was terminated before the onset of shivering. Skin blood flow was monitored by laser-Doppler flowmetry and arterial pressure by finger photoplethysmography. In all experiments, cutaneous vasoconstriction began immediately with the onset of cooling, and cutaneous vascular conductance (CVC) decreased progressively with decreasing Tsk. Regression analysis of the relationship of CVC to Tsk showed no difference in slope between phases (low-hormone phase: 17.67 ± 5.57; high-hormone phase: 17.40 ± 8.00 %baseline/°C; P > 0.05). Additional studies involving local blockade confirmed this response as being solely due to the adrenergic vasoconstrictor system. Waking oral temperature (Tor) was significantly higher on high-hormone vs. low-hormone days (36.60 ± 0.11 vs. 36.37 ± 0.09 °C, respectively; P < 0.02). Integrative analysis of CVC in terms of simultaneous values for Tsk and Tor showed that the cutaneous vasoconstrictor response was shifted in the high-hormone phase such that a higher Tor was maintained throughout cooling ( P < 0.05). Thus reflex thermoregulatory control of the cutaneous vasoconstrictor system is shifted to higher internal temperatures by exogenous female reproductive hormones.

scholarly journals Nitric oxide and cutaneous active vasodilation during heat stress in humans

1998 ◽  
Vol 85 (3) ◽  
pp. 824-829 ◽  
Author(s):  
D. L. Kellogg ◽  
C. G. Crandall ◽  
Y. Liu ◽  
N. Charkoudian ◽  
J. M. Johnson
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Laser Doppler Flowmetry ◽  
Sweat Rate ◽  
Ringer Solution ◽  
No Synthase ◽  
Laser Doppler ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Cutaneous Vascular Conductance

Whether nitric oxide (NO) is involved in cutaneous active vasodilation during hyperthermia in humans is unclear. We tested for a role of NO in this process during heat stress (water-perfused suits) in seven healthy subjects. Two forearm sites were instrumented with intradermal microdialysis probes. One site was perfused with the NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME) dissolved in Ringer solution to abolish NO production. The other site was perfused with Ringer solution only. At those sites, skin blood flow (laser-Doppler flowmetry) and sweat rate were simultaneously and continuously monitored. Cutaneous vascular conductance, calculated from laser-Doppler flowmetry and mean arterial pressure, was normalized to maximal levels as achieved by perfusion with the NO donor nitroprusside through the microdialysis probes. Under normothermic conditions,l-NAME did not significantly reduce cutaneous vascular conductance. During hyperthermia, with skin temperature held at 38–38.5°C, internal temperature rose from 36.66 ± 0.10 to 37.34 ± 0.06°C ( P < 0.01). Cutaneous vascular conductance at untreated sites increased from 12 ± 2 to 44 ± 5% of maximum, but only rose from 13 ± 2 to 30 ± 5% of maximum at l-NAME-treated sites ( P < 0.05 between sites) during heat stress. l-NAME had no effect on sweat rate ( P > 0.05). Thus cutaneous active vasodilation requires functional NO synthase to achieve full expression.

Effects of obesity and mild hypohydration on local sweating and cutaneous vascular responses during passive heat stress in females

2016 ◽  
Vol 41 (8) ◽  
pp. 879-887 ◽  
Author(s):  
Nicole E. Moyen ◽  
Jenna M. Burchfield ◽  
Cory L. Butts ◽  
Jordan M. Glenn ◽  
Matthew A. Tucker ◽  
...  
Keyword(s):  
Heat Stress ◽  
Steady State ◽  
Body Fat ◽  
Urine Specific Gravity ◽  
Fluid Restriction ◽  
Vascular Conductance ◽  
Mean Body Temperature ◽  
Doppler Flowmetry ◽  
Vascular Responses ◽  
Cutaneous Vascular Conductance

The purpose of this study was to evaluate the effect of obesity and mild hypohydration on local sweating (LSR) and cutaneous vascular conductance (CVC) responses during passive heat stress in females. Thirteen obese (age, 24 ± 4 years; 45.4% ± 5.2% body fat) and 12 nonobese (age, 22 ± 2 years; 25.1% ± 3.9% body fat) females were passively heated (1.0 °C rectal temperature increase) while either euhydrated (EUHY) or mildly hypohydrated (HYPO; via fluid restriction). Chest and forearm LSR (ventilated capsule) and CVC (Laser Doppler flowmetry) onset, sensitivity, and plateau/steady state were recorded as mean body temperature increased (ΔTb). Participants began trials EUHY (urine specific gravity, Usg = 1.009 ± 0.006) or HYPO (Usg = 1.025 ± 0.004; p < 0.05), and remained EUHY or HYPO. Independent of obesity, HYPO decreased sweat sensitivity at the chest (HYPO = 0.79 ± 0.35, EUHY = 0.95 ± 0.39 Δmg·min−1·cm−2/°C ΔTb) and forearm (HYPO = 0.82 ± 0.39, EUHY = 1.06 ± 0.34 Δmg·min−1·cm−2/°C ΔTb); forearm LSR plateau was also decreased (HYPO = 0.66 ± 0.19, EUHY = 0.78 ± 0.23 mg·min−1·cm−2; all p < 0.05). Overall, obese females had lower chest-sweat sensitivity (0.72 ± 0.35 vs. 1.01 ± 0.33 Δmg·min−1·cm−2/°C ΔTb) and plateau (0.55 ± 0.27 vs. 0.80 ± 0.25 mg·min−1·cm−2; p < 0.05). While hypohydrated, obese females had a lower chest LSR (p < 0.05) versus nonobese females midway (0.45 ± 0.26 vs. 0.73 ± 0.23 mg·min−1·cm−2) and at the end (0.53 ± 0.27 vs. 0.81 ± 0.24 mg·min−1·cm−2) of heating. Furthermore, HYPO (relative to the EUHY trials) led to a greater decrease in CVC sensitivity in obese (–28 ± 27 Δ% maximal CVC/°C ΔTb) versus nonobese females (+9.2 ± 33 Δ% maximal CVC/°C ΔTb; p < 0.05). In conclusion, mild hypohydration impairs females’ sweating responses during passive heat stress, and this effect is exacerbated when obese.

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.

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