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PubMed1995

Desflurane slightly increases the sweating threshold but produces marked, nonlinear decreases in the vasoconstriction and shivering thresholds.

BACKGROUND: Shivering is rare during general anesthesia. This observation suggests that anesthetics profoundly impair shivering. However, the effects of surgical doses of volatile anesthetics on control of shivering have yet to be evaluated. Furthermore, the effects of desflurane on sweating and thermoregulatory vasoconstriction remain unknown. Accordingly, the authors determined the concentration-dependent effects of desflurane on sweating, vasoconstriction, and shivering. METHODS: Nine volunteers each were studied on three randomly ordered days: (1) control (no anesthesia); (2) a target end-tidal desflurane concentration of 0.5 minimum alveolar concentration (MAC; 3.5%); and (3) a target concentration of 0.8 MAC (5.6%). Each day, volunteers were warmed until sweating was induced and subsequently cooled until peripheral vasoconstriction and shivering was observed. Changes in skin temperature were arithmetically compensated using the established linear cutaneous contributions to control of each response. From the calculated thresholds (core temperatures triggering responses at a designated skin temperature of 34 degrees C), the concentration-response relationship was determined. RESULTS: Desflurane significantly and linearly increased the sweating threshold from 37.1 +/- 0.3 degrees C on the control day (mean +/- SD), to 37.6 +/- 0.4 degrees C at 0.5 MAC, and to 38.1 +/- 0.3 degrees C at 0.8 MAC. Desflurane significantly, but nonlinearly, reduced the vasoconstriction and shivering thresholds. The sweating-to-vasoconstriction (interthreshold) range thus increased from 0.5 +/- 0.3 degrees C to 2.3 +/- 0.7 degrees C at 0.5 MAC and further to 4.6 +/- 2.0 degrees C at 0.8 MAC. The vasoconstriction-to-shivering range (difference between the respective thresholds) remained between 1.1 and 1.5 degrees C on the three study days. CONCLUSIONS: The observed linear increase in the sweating threshold was similar in pattern and magnitude to that produced by most general anesthetics. The approximately 3 degrees C reduction in the vasoconstriction threshold by 0.8 MAC desflurane was similar to that observed previously during isoflurane and propofol anesthesia. However, the threshold was reduced less than expected at 0.5 MAC, suggesting that the dose-response relationship for vasoconstriction is nonlinear. Shivering was induced without difficulty in this study although the response is rare in surgical patients. It is likely that shivering during general anesthesia is rare because thermoregulatory vasoconstriction usually prevents body temperature from decreasing the required additional 1-1.5 degrees C.

Adult↗

PubMed1992

Adrenaline-induced local sweating and vasoconstrictive responses in atopic skin.

Sweating and vasoconstrictive responses to intradermal injections of adrenaline were studied in the normal-looking back skin of young adult males with atopic dermatitis (AD) and in non-atopic controls using five concentrations of adrenaline, and further in a subgroup of subjects with dry-looking AD skin using two concentrations of adrenaline. The sweating responses were measured with an evaporimeter and the area of blanching determined with planimetry. The maximal sweating response in the AD group was elicited with the suprathreshold concentration of 5 x 10(-6) mol/l and in the non-atopic group with a 10-fold higher concentration. At the three higher concentrations the sweat rates levelled out in both groups and remained at a lower level in AD subjects. The sweating responses in dry-looking AD skin were lower than in non-atopics (P less than 0.001) and were also lower than in those with AD normal-looking skin (P less than 0.05) with both concentrations. In contrast to sweating, the vasoconstrictive reactions showed similar dose-dependent increases with all tested concentrations in AD patients with normal-looking skin and in the non-atopic controls. In patients with dry AD skin the vasoconstrictive responses were also similar to those in non-atopic controls.

Adult↗

PubMed1996

Identification of electrophysiologically-active compounds for the malaria mosquito, Anopheles gambiae, in human sweat extracts.

Human sweat samples were chemically fractionated into acid and non-acid components. The most abundant volatile compounds present in the fractions were identified by linked gas chromatography mass spectrometry. The acid fractions were found to be composed of a range of twenty aliphatic and three aromatic carboxylic acids ranging, on average, from 0.02 to 20 micrograms per ml of sweat sampled. Non-acid fractions were found to contain: 6-methyl-5-hepten-2-one, 1-octen-3-ol, decanal, benzyl alcohol, dimethylsulphone, phenylethanol, phenol and 4-methylphenol, collectively amounting to 0.1 and 3 micrograms per ml of sweat. The major component of sweat was found to be L-lactic acid which constituted from 1 to 5 mg/ml. Using the intact antennae of the anthropophilic malaria vector mosquito Anopheles gambiae Giles, the peripheral olfactory activities of compounds identified in the sweat fractions were investigated by electroantennography (EAG). Short-chain saturated carboxylic acids, methanoic, ethanoic, propanoic, butanoic, pentanoic and hexanoic acids were found to elicit significantly larger EAG responses than longer chain saturated carboxylic acids from female An.gambiae. For a given dose the largest amplitude EAG response was elicited by methanoic acid. Pentanoic acid elicited larger EAG responses than either butanoic or hexanoic acids. Two non-acidic compounds, 1-octen-3-ol and 4-methylphenol, were found to elicit significant dose-dependent EAG responses from female An.gambiae. 1-Octen-3-ol elicited larger EAG responses than 4-methylphenol for a given dose, but both compounds elicited smaller EAG responses than the same dose of C1-C6 straight-chain aliphatic carboxylic acids. The possible behavioural significance of the EAG-active compounds identified in human sweat samples is discussed.

Adult↗

PubMed1992

Sebaceous gland and sweat gland carcinomas of the skin. Clinicopathological study and significance of c-erbB-2 oncoprotein expression.

Thirteen sebaceous gland carcinomas and 10 sweat gland carcinomas were examined to elucidate any important histological parameters influencing their prognosis, and the relationship between immunohistochemical expressions of c-erbB-2 oncoprotein and survival of the patients was analyzed. Sebaceous gland carcinomas with vacuolated cytoplasm in more than 50% of whole tumor area, with necrosis, and without lymphoid cell infiltration in tumor nests and stroma had a higher incidence of tumor recurrence and tumor-related death than tumors with vacuolated cytoplasm in 50% or less of whole tumor area (p < 0.01), without necrosis, and with lymphoid cell infiltration in tumor nest and stroma (p < 0.05). Sweat gland carcinomas of all cases with fatal outcomes demonstrated tubular differentiation in 20% or less of whole tumor area, lymphatic permeation and desmoplastic reaction. Three sebaceous gland carcinomas and three sweat gland carcinomas were positive for c-erbB-2 oncoprotein. Two of three sebaceous gland carcinomas, and all three sweat gland carcinomas developed tumor recurrence and ended in tumor-related deaths. Sweat gland carcinomas with c-erbB-2 expression had significantly shorter survival than those with negative immunostain (p < 0.01). Cytoplasmic appearance, tumor necrosis, and lymphoid cell infiltration in tumor nests and stroma of sebaceous gland carcinoma, and tubular differentiation, lymphatic permeation, and growth patterns of sweat gland carcinoma are considered to closely correlate to the prognosis. Immunohistochemically detected c-erbB-2 oncoprotein may be an indicator of bad prognosis.

Adolescent↗

PubMed2001

Absence of arterial baroreflex modulation of skin sympathetic activity and sweat rate during whole-body heating in humans.

1. Prior findings suggest that baroreflexes are capable of modulating skin blood flow, but the effects of baroreceptor loading/unloading on sweating are less clear. Therefore, this project tested the hypothesis that pharmacologically induced alterations in arterial blood pressure in heated humans would lead to baroreflex-mediated changes in both skin sympathetic nerve activity (SSNA) and sweat rate. 2. In seven subjects mean arterial blood pressure was lowered (approximately 8 mmHg) and then raised (approximately 13 mmHg) by bolus injections of sodium nitroprusside and phenylephrine, respectively. Moreover, in a separate protocol, arterial blood pressure was reduced via steady-state administration of sodium nitroprusside. In both normothermia and heat-stress conditions the following responses were monitored: sublingual and mean skin temperatures, heart rate, beat-by-beat blood pressure, skin blood flow (laser-Doppler flowmetry), local sweat rate and SSNA (microneurography from peroneal nerve). 3. Whole-body heating increased skin and sublingual temperatures, heart rate, cutaneous blood flow, sweat rate and SSNA, but did not change arterial blood pressure. Heart rate was significantly elevated (from 74 +/- 3 to 92 +/- 4 beats x min(-1); P < 0.001) during bolus sodium nitroprusside-induced reductions in blood pressure, and significantly reduced (from 92 +/- 4 to 68 +/- 4 beats x min(-1); P < 0.001) during bolus phenylephrine-induced elevations in blood pressure, thereby demonstrating normal baroreflex function in these subjects. 4. Neither SSNA nor sweat rate was altered by rapid (bolus infusion) or sustained (steady-state infusion) changes in blood pressure regardless of the thermal condition. 5. These data suggest that SSNA and sweat rate are not modulated by arterial baroreflexes in normothermic or moderately heated individuals.

Adult↗

PubMed1978

Excretion of antiepileptic drugs in sweat.

In eight epileptic patients receiving chronic antiepileptic treatment, a study of the excretion in sweat of phenytoin, phenobarbitone and carbamazepine was performed. All three drugs were found to be present in sweat. Phenytoin sweat concentration was found to correspond to the free fraction in plasma and to be independent of sweat flow. Phenobarbitone sweat concentration was found to increase with increasing sweat flow. Regarding drug level monitoring it is proposed that under changing climatic conditions the phenomenon may be of clinical significance.

Adolescent↗

PubMed1986

Malnutrition: a cause of elevated sweat chloride concentration.

In order to document the frequency and causes of elevated sweat chlorides we reviewed all sweat chloride determinations performed over a 2-year period. Seven hundred and thirty-five quantitative tests were performed. Three hundred and three positive or borderline results were obtained from 133 patients. Thirty-three of these patients did not have clinical evidence of CF. Fourteen of them (42%) suffered from malnutrition or growth stunting when tested. The remaining patients who were normally nourished, represented a very heterogeneous group with no unifying diagnosis. Initial sweat chlorides in 11/14 malnourished children were in the abnormal range (greater than 60 mmol/l). These tended to revert to normal coincident with improvement in nutritional status. Less remarkable elevations in sweat chloride levels were noted in the normally nourished patients, since almost 50% (9/19) were in the intermediate range (50-60 mmol/l). We conclude that malnutrition can be the cause of elevated sweat chlorides, which may lead to an erroneous diagnosis of cystic fibrosis. Clinicians should be aware of this association and adhere to strict criteria for the diagnosis of cystic fibrosis. Also, repeated sweat chloride determinations should be obtained, preferably following re-nutrition.

Adolescent↗

PubMed1973

The regional distribution of emotional sweating in man.

1. Emotional sweating was induced in normal subjects by mental arithmetic at environmental temperatures of 29 and 26 degrees C and estimated from continuous records of body weight loss.2. The sweat output from four independent regions of the body - (a) the head and neck, (b) the arms and legs, (c) the trunk, and (d) the hands and feet - was studied separately, the remainder of the body being covered in each case by plastic bags. The evaporative water loss from each skin region increased markedly during mental arithmetic.3. The sweat contribution from each region was a substantial fraction of the total body sweat response and appeared to be roughly proportional to the calculated number of sweat glands in each region.4. There is no evidence from these experiments to indicate that the sweat glands of the skin of the hands and feet behave differently to those of the skin of the rest of the body in response to emotional stress.

Adult↗

PubMed1997

Comparison of sweat rate measured by a pouch collector and a hygrometric technique during exercise.

Measurements of local sweat rate (back) determined with a closed-pouch collector made of polyethylene (110 cm2) were compared with those obtained from a ventilated capsule using an infrared photometric hygrometer technique. Eight young male subjects underwent three exercise sessions each for 60 min at 45% VO2max on a cycle ergometer at an ambient temperature of 35 degrees C and 35% relative humidity. When the onset and transient sweating periods (0-20 min) are excluded from calculations, the difference between the mean values obtained by the collector and the sweat capsule during the 20-60 time period is only 0.06 +/- 0.04 mg x cm-2 x min-1 (5%). Although a significant correlation (r = .74, p < .05) was obtained between methods, individual differences in sweat-rate measurements varied on average +/-0.22 mg x cm-2 x min-1 (+/-19%). Designed more specifically for sweat-content analysis, the pouch collector may serve as a satisfactory field method to approximate the local sweat rate and excretion induced by prolonged exercise in a hot environment.

Adult↗

PubMed1990

Regulation of Cl- permeability in normal and cystic fibrosis sweat duct cells.

Reabsorptive cells of the human sweat gland normally exhibit a high basal Cl- permeability but are markedly impermeable to Cl- in cystic fibrosis (CF). We examined the possibility that the reduced basal Cl- permeability of CF sweat duct cells in primary culture is due to a defective regulation of plasma membrane Cl- permeability by prostaglandin E2 (PGE2), which is endogenously produced by cultured sweat duct cells. The macroscopic Cl- permeabilities of normal and CF sweat duct cells were assessed using a halide-specific fluorescent dye, 6-methoxy-N-(3-sulfopropyl)quinolinium, in combination with fluorescence digital-imaging microscopy. The Cl- and Br- permeabilities of normal sweat duct cells were markedly reduced by inhibiting endogenous PGE2 production with indomethacin. This inhibition of Cl- permeability by indomethacin was largely reversed by the addition of PGE2 (10 nM to 1 microM), but not forskolin. Conversely, PGE2 failed to stimulate the low Cl- permeabilities of sweat duct cells cultured from CF subjects. Our results support the following conclusions: 1) a defective regulation of Cl- permeability in CF is a feature of reabsorptive as well as secretory epithelial cells, and 2) the nature of this regulatory defect extends beyond altered Cl- permeability regulation by adenosine 3',5'-cyclic monophosphate-dependent protein kinase.

Cell Membrane Permeability↗

PubMed1986

Proteolytic enzymes in human eccrine sweat: a screening study.

Thermally induced human eccrine sweat was collected both by simple scraping (SS) and by a polyethylene sweat collector that covered the Vaseline-coated skin of the back to minimize epidermal contamination (CS, clean sweat). Using synthetic chromogenic Kabi S-series substrates, we demonstrated a variety of proteases in both SS and CS, the former being higher than the latter to varying extents. The higher enzyme activity in SS is mainly due to epidermal contamination because abundant protease activity was eluted from the nonperspiring stripped and unstripped skin in vivo and from the stripped stratum corneum itself. The electrophoretic separation of sweat protein has shown that CS contains at least 7 and SS 15 gelatinolytic proteinases. Although some CS proteinases could be derived from the sweat duct, the sweat secretory coil itself is responsible for at least two proteinases at 78 and 25 kilodaltons. The identity and function of these enzymes remain to be studied.

Caseins↗

PubMed1977

Increase in sweating sensitivity by endurance conditioning in man.

Sweating sensitivity has been evaluated at rest in 10 competitive athletes (cross-country skiers and swimmers). Three sedentary men underwent a 3-mo period of endurance training in a temperate climate, (dry bulb temperature (Tdb): 18 degrees C) and had their sweating sensitivity measured before and after the training period. Mean maximum oxygen uptake (Vo2max, ml.min(-1).kg(-1)) was: skiers: 66.5; swimmers 65.8; sedentary men, pretraining 40.9; posttraining: 48.3 (+18%). Sweat output of athletes under a given stress (passive heating) was markedly higher than that of sedentary men. Skiers exhibited a high level of heat tolerance and were better acclimatized than swimmers, although they had never experienced exposure to heat. The increase in Vo2max of sedentary men was accompanied by 1) an increase in sweating sensitivity with a decrease of body heat storage at steady state (pretraining: 5.4 kJ.kg(-1); posttraining: 3.5 kJ.kg(-1); P less than 0.05); 2) significant shift down the temperature scale with reduced rectal temperature (Tre) for sweat onset; 3) an increase of gain constants of sweating (W.m-2 degrees C(-1) (pretraining: 168; posttraining: 269; gain constant of swimmers: 222). It was suggested that endurance training in cold or temperate conditions with significant increase of Vo2max could act on the thermoregulatory function in a way similar to body heating procedures, such as work in heat, and could contribute to heat acclimatization.

Acclimatization↗

PubMed1980

An electrocapillary flowmeter usable as a quantitative sweat detector.

A quantitative sweat detector was devised as part of a noninvasive portable warning apparatus intended for the surveillance of unstable insulin-treated diabetics who may have nocturnal hypoglycemic attacks. The sweat sensor consists of a pair of electrodes embedded in a porous material that is infiltrated under capillary drive by sweat as it oozes out of the skin. It was shown that the detector is almost insensitive to insensible perspiration but undergoes graded variation of impedance as it is filled with sweat. It thus works as a transducer of sweat flux (flow rate through unit skin area) as long as the porous material is not saturated. This device has already proved useful as a hypogycemic alarm and could certainly be used for the measurement of sweating rate in place of more cumbersome devices involving ventilated chambers.

Adult↗

PubMed1987

Effect of age on heat-activated sweat gland density and flow during exercise in dry heat.

Physiological responses of eight postmenopausal older women (age 52-62 yr) and eight younger women (age 20-30 yr) were compared during moderate intensity exercise in a hot dry environment (48 degrees C dry bulb, 25 degrees C wet bulb). The age groups were matched on the basis of maximal O2 consumption (VO2max), body surface area, and body fatness. After heat acclimation the women walked at 40% VO2max for up to 2 h in the hot dry environment while heart rate (HR), rectal temperature (Tre), mean skin temperature (Tsk), whole-body sweating rate (Msw), and local sweating rates (msw; forearm, chest, and scapula) were measured. Additionally, the density of heat-activated sweat glands (HASG) was determined and average sweat gland flow (SGF) was calculated for the scapular area. Although no differences between age groups were found in HR response (when analyzed as percent of maximal HR) or Tsk, the older women had a significantly higher Tre throughout the heat-exercise session. The greater heat storage of the older women may be explained by their significantly lower Msw and msw. There were no differences between the younger and older women in the density of HASG after 30 min; therefore, the lower msw reflects a diminished output per HASG rather than a decrease in the number of sweat glands recruited. The diminished thermoregulatory ability of the older women, unrelated to differences in VO2max, appears to reflect either 1) a diminished response of the sweat glands to central and/or peripheral stimuli, or 2) an age-related structural alteration in the eccrine glands or surrounding skin cells.

Adult↗

PubMed1997

Whole body sweat collection in humans: an improved method with preliminary data on electrolyte content.

Previous methods used to collect human sweat for electrolyte analysis have been criticized because they involve only regional sampling or because of methodological problems associated with whole body-washdown techniques. An improved method for collection of whole body sweat from exercising subjects is described. It involved construction of a plastic frame that supports a large plastic bag within which the subject exercises. The subject and the equipment are washed with distilled, deionized water before exercise begins. After exercise is completed, the subject and equipment are again washed with water containing a marker not present in sweat (ammonium sulfate). Total sweat loss is calculated from the change in body mass, and the volume of sweat not evaporated is calculated from dilution of the added marker. Recovery of added water was 102 +/- 2% (SD) of the added volume, and recovery of added electrolytes was 99 +/- 2% for sodium, 98 +/- 9% for potassium, and 101 +/- 4% for chloride. Repeated trials (n = 4) on five subjects to establish the reproducibility of the method gave a coefficient of variation of 17 +/- 5% for sodium, 23 +/- 6% for potassium, and 15 +/- 6% for chloride. These values include the biological variability between trials as well as the error within the method. The biological variability thus appears to be far greater than the methodological error. Normal values for the composition of sweat induced by exercise in a hot, humid environment in healthy young men and women were (in mM) 50.8 +/- 16.5 sodium, 4.8 +/- 1.6 potassium, 1.3 +/- 0.9 calcium, 0.5 +/- 0.5 magnesium, and 46.6 +/- 13.1 chloride.

Adult↗

PubMed2005

Role of nitric oxide in methacholine-induced sweating and vasodilation in human skin.

The purpose of this study was to determine whether the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) demonstrates significant muscarinic-receptor antagonism during methacholine (MCh)-stimulated sweating in human forearm skin. Three intradermal microdialysis probes were placed in the skin of eight healthy adults (4 men and 4 women). MCh in the range of 0.033-243 mM in nine steps was perfused through a microdialysis probe with and without the presence of the nitric oxide synthase inhibitor L-NAME (10 mM) or the L-arginine analog NG-monomethyl-L-arginine (L-NMMA; 10 mM). Local sweat rate (sweat rate) and skin blood flow (laser-Doppler velocimetry) were measured directly over each microdialysis probe. We observed similar resting sweat rates at MCh only, MCh and L-NAME, and MCh and L-NMMA sites averaging 0.175 +/- 0.029, 0.186 +/- 0.034, and 0.139 +/- 0.027 mg x min(-1) x cm(-2), respectively. Peak sweat rate (0.46 +/- 0.11, 0.56 +/- 0.16, and 0.53 +/- 0.16. mg x min(-1) x cm(-2)) was also similar among all three sites. MCh produced a sigmoid-shape dose-response curve and 50% of the maximal attainable response (0.42 +/- 0.14 mM for MCh only) was shifted rightward shift in the presence of L-NAME or L-NMMA (2.88 +/- 0.79 and 3.91 +/- 1.14 mM, respectively; P < 0.05). These results indicate that nitric oxide acts to augment MCh-stimulated sweat gland function in human skin. In addition, L-NAME consistently blunted the MCh-induced vasodilation, whereas L-NMMA did not. These data support the hypothesis that muscarinic-induced dilation in cutaneous blood vessels is not mediated by nitric oxide production and that the role of L-NAME in attenuating acetylcholine-induced vasodilation may be due to its potential to act as a muscarinic-receptor antagonist.

Adult↗

PubMed2005

Nonthermoregulatory control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in women.

The purpose of the study was to examine the effect of 1) active (loadless pedaling), 2) passive (assisted pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), cutaneous vascular conductance (CVC), and sweat rate during recovery after 15 min of dynamic exercise in women. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, CVC, and sweating during exercise recovery. Ten female subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 20 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (Tsk), esophageal temperature (Tes), skin blood flow, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, 15, and 20 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active recovery mode, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values (P < 0.05). The passive mode was equally as effective as the active mode in maintaining MAP. Sweat rate was different among all modes after 12 min of recovery (P < 0.05). TPR during active recovery remained significantly lower than during recovery in the inactive mode (P < 0.05). No differences in either Tes or Tsk were observed among conditions. The results indicate that CVC can be modulated by central command and possibly cardiopulmonary baroreceptors in women. However, differences in sweat rate may be influenced by factors such as central command, mechanoreceptor stimulation, or cardiopulmonary baroreceptors.

Adult↗

PubMed2006

Neural control and mechanisms of eccrine sweating during heat stress and exercise.

In humans, evaporative heat loss from eccrine sweat glands is critical for thermoregulation during exercise and/or exposure to hot environmental conditions, particularly when environmental temperature is greater than skin temperature. Since the time of the ancient Greeks, the significance of sweating has been recognized, whereas our understanding of the mechanisms and controllers of sweating has largely developed during the past century. This review initially focuses on the basic mechanisms of eccrine sweat secretion during heat stress and/or exercise along with a review of the primary controllers of thermoregulatory sweating (i.e., internal and skin temperatures). This is followed by a review of key nonthermal factors associated with prolonged heat stress and exercise that have been proposed to modulate the sweating response. Finally, mechanisms pertaining to the effects of heat acclimation and microgravity exposure are presented.

Adaptation, Physiological↗