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PubMed2005

Morphological and distribution characteristics of sweat glands in hypertrophic scar and their possible effects on sweat gland regeneration.

BACKGROUND: In hypertrophic scar tissue, no sweet gland and hair follicle exist usually because of the dermal and epidermal damage in extensive thermal skin injury, thus imparing regulation of body temperature. This study was designed to reveal the morphological and distributional characteristics of the sweat glands in normal skin and hypertrophic scar obtained from children and adults, and to study the possible interfering effects of the scar on regeneration of the sweat gland after burn injury. METHODS: Biopsies of hypertrophic scar were taken from four children (4 - 10 years) and four adults (35 - 51 years). Normal, uninjured full-thickness skin adjacent to the scar of each patient was used as control. Keratin 19 (K19) was used as the marker for epidermal stem cells and secretory portion of the sweat glands, and keratin 14 (K14) for the tube portion, respectively. Immunohistochemical and histological evaluations were performed. RESULTS: Histological and immunohistochemical staining of skin tissue sections from both the children and adults showed K19 positive cells in the basement membrane of epidermis of normal skin. These cells were seen only single layer and arranged regularly. The secretory or duct portion of the eccrine sweat glands was situated in the dermis and epidermal layer. However, in the scar tissue, K19 positive cells were scant in the basal layer, and the anatomic location of the secretory portion of sweat glands changed. They were located between the border of the scar and reticular layer of the dermis. These secretory portions of sweat glands were expanded and were organized irregularly. But a few K14 positive cells were scattered in the scar tissues in cyclic form. CONCLUSIONS: There are some residual sweat glands in scar tissues, in which the regeneration process of active sweat glands is present. Possibly the sweat glands could regenerate from adult epidermal stem cells or residual sweat glands in the wound bed after burn injury.

Adult↗
PubMedDate not supplied

Prevalence and predictors of night sweats, day sweats, and hot flashes in older primary care patients: an OKPRN study.

PURPOSE: We wanted to estimate the prevalence of night sweats, day sweats, and hot flashes in older primary care patients and identify associated factors. METHODS: We undertook a cross-sectional study of patients older than 64 years recruited from the practices of 23 family physicians. Variables included sociodemographic information, health habits, chronic medical problems, symptoms, quality of life, and the degree to which patients were bothered by night sweats, daytime sweating, and hot flashes. RESULTS: Among the 795 patients, 10% reported being bothered by night sweats, 9% by day sweats, and 8% by hot flashes. Eighteen percent reported at least 1 of these symptoms. The 3 symptoms were strongly correlated. Factors associated with night sweats in the multivariate models were age (odds ratio [OR] 0.94/y; 95% confidence interval [CI], 0.89-0.98), fever (OR 12.60; 95% CI, 6.58-24.14), muscle cramps (OR 2.84; 95% CI, 1.53-5.24), numbness of hands and feet (OR 3.34; 95% CI, 1.92-5.81), impaired vision (OR 2.45; 95% CI, 1.41-4.27), and hearing loss (OR 1.84; 95% CI, 1.03-3.27). Day sweats were associated with fever (OR 4.10; 95% CI, 2.14-7.87), restless legs (OR 3.22; 95% CI, 1.76-5.89), lightheadedness (OR 2.24; 95% CI, 1.30-3.88), and diabetes (OR 2.19; 95% CI, 1.22-3.92). Hot flashes were associated with nonwhite race (OR 3.10; 95% CI, 1.60-5.98), fever (OR 3.98; 95% CI, 1.97-8.04), bone pain (OR 2.31; CI 95%: 1.30-4.08), impaired vision (OR 2.12; 95% CI, 1.19-3.79), and nervous spells (OR 1.87; 95% CI, 1.01-3.46). All 3 symptoms were associated with reduced quality of life. CONCLUSION: Many older patients are bothered by night sweats, day sweats, and hot flashes. Though these symptoms are similar and related, they have somewhat different associations with other variables. Clinical evaluation should include questions about febrile illnesses, sensory deficits, anxiety, depression, pain, muscle cramps, and restless legs syndrome.

Aged↗
PubMed1987

Development and properties of the secretory response in rat sweat glands: relationship to the induction of cholinergic function in sweat gland innervation.

Previous studies suggest that the sympathetic innervation of the sweat glands in the rat is initially noradrenergic and during development undergoes a transition in neurotransmitter phenotype to become cholinergic. To characterize this system and its development further, we have examined the adrenergic and cholinergic components of the secretory response in adult and immature rats and have studied the onset of sweating in the plantar sweat glands of developing rats. Stimulation of the sciatic nerve in adult rats elicited a secretory response which was completely blocked by the cholinergic antagonist, atropine, and was unaffected by adrenergic antagonists, indicating that nerve-evoked secretion was cholinergic. In adult rats, the sweat glands were quite sensitive to cholinergic agonists. In addition to acetylcholine, the mature sweat gland innervation contains vasoactive intestinal peptide (VIP). In some rats, the injection of VIP alone elicited a secretory response which was blocked by atropine, suggesting that the response to VIP was mediated cholinergically. In contrast to cholinergic agonists, the glands responded relatively infrequently and with reduced volumes of sweat to the alpha- and beta-adrenergic agonists 6-fluoronorepinephrine and isoproterenol. However, when VIP, which is a potent vasodilator, was simultaneously injected with adrenergic agonists, glands in many of the injected footpads exhibited a secretory response. The response to adrenergic agonists in combination with VIP was reduced by atropine and by phentolamine plus propranolol, but was blocked completely only by a combination of the three antagonists, indicating that both adrenergic and cholinergic mechanisms were involved. In immature rats, sweating evoked by nerve stimulation first appeared at 14 days of age in 25% of the rats tested. Both the percentage of rats sweating and the number of active glands increased rapidly. At 16 days, 50% of the rats tested exhibited some active glands, and by 21 days all rats tested exhibited a secretory response. In 16-day-old rats, nerve-evoked sweating was almost completely inhibited by local injection of 1 microM atropine, but was unaffected by phentolamine and propranolol in concentrations up to 10 microM. Similarly, the glands were sensitive to 10 microM muscarine, but they exhibited no secretory response to the alpha-adrenergic agonists, clonidine and 6-fluoronorepinephrine, nor to the beta-adrenergic agonist, isoproterenol, at concentrations up to 50 microM. The simultaneous injection of VIP with adrenergic agonists did not reveal an adrenergically mediated secretory response in 16-day-old animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1988

Identification of secretory immunoglobulin A in human sweat and sweat glands.

Secretory immunoglobulin A (sIgA) plays an important role in local immune defense mechanisms. Although skin is always exposed to external antigens, the role of local immune defenses involving sIgA in the skin has not been adequately studied. In order to evaluate the presence of sIgA in sweat, we have measured the concentration of sIgA in human sweat by enzyme immunoassay and have localized the components of sIgA in the sweat glands of human axillary skin. The concentration of sIgA in sweat was found to be 10 times higher in men than in women (13.0 +/- 0.9 micrograms/ml versus 1.6 +/- 0.9 micrograms/ml). Secretory component (SC) was localized immunohistochemically in protein synthetic organelles, such as the perinuclear spaces and Golgi complex, in cytoplasmic vesicles, and along the external surface membranes of mucous cells on the terminal segment of eccrine sweat glands. IgA and J chain were present in plasma cells in the protein synthetic organelles. The luminal aspects of eccrine sweat ducts also strongly express SC, as well as IgA and J chain. Neither SC, IgA, or J chain were identified in epithelial cells of apocrine sweat glands. These findings are consistent with the theory that J chain complexed with dimeric IgA is synthesized in plasma cells and is transported by SC-mediated endocytosis transfer across mucous cells of eccrine sweat glands and thus into sweat.

Adult↗
PubMed1995

Sweating rate and sweat composition during exercise and recovery in ambient heat and humidity.

The objective of this study was to determine the composition and extent of sweat losses during submaximal exercise under hot and humid conditions and to compare these findings with the same exercise protocol conducted under cool, dry and hot, dry conditions. Five Thoroughbred horses (age 3 to 6) completed exercise tests under each of 3 environmental conditions in random order: cool, dry (CD), room temperature (T) = 20 degrees C, relative humidity (RH) = 45-55%; hot, dry (HD), T = 32-34 degrees C, RH = 45-55%; and hot, humid (HH), T = 32-34 degrees C, RH = 80-85%. Horses exercised at 50% of their predetermined VO2max on a treadmill set at a 10% slope until attainment of a pulmonary artery blood temperature of 41.5 degrees C followed by a 60 min recovery. Sweat was collected from a sealed polyethylene pouch enclosing a 150 cm2 area on the lateral thorax. During exercise and the first 30 min of recovery, sweat fluid losses were 7.9 +/- 0.7 litres, 9.9 +/- 0.5 litres and 6.6 +/- 1.2 litres (mean +/- s.e.m.) for CD, HD and HH, respectively. Sweating rate (SR), calculated from sweat volume per unit area of enclosed skin, was lowest in CD and similar in HD and HH during exercise such that at end of exercise in HH (16.5 min) calculated sweat losses were approximately 5% and 32% higher than in HD and CD, respectively. In recovery, SR declined in all conditions but was significantly lower in CD (P < 0.05). Sweating was detectable until 30 min recovery in CD, 45 min recovery in HD and 60 min recovery in HH. Sweat composition and osmolality was different under the 3 environmental conditions and changed gradually during exercise and recovery in all conditions. Osmolality and [Na] was highest in HD and lowest in CD. During exercise, [Na] increased with increasing SR. Although exercise duration was significantly decreased in HH (16.5 +/- 1 min) when compared to HD (28 +/- 2 min) and CD (37 +/- 2 min), fluid and ion losses in HH were comparable to those in HD as a result of a high SR and prolonged sweating during recovery.

Animals↗
PubMed1976

Relationship between evaporation rate of sweat and mean sweating rate.

The rate of evaporation of sweat under a step change of ambient temperature (30-45 degrees C) was compared with the mean sweating rate (MSR) computed from five simultaneous resistance hygrometric measurements. Empirical equations derived for the conditions studied enabled a direct conversion from hygrometric measurements into real evaporative sweat losses and skin wetness for all phases of sweat evaporation. From five chosen skin areas, forehead, forearm, chest, thigh, and calf, it was found that none of these sites gave a local sweating response close to the MSR. In the subjects with a forehead sweating rate within +/- 39% of the MSR, at least four hygrometric sensors were needed to predict the rate of sweat evaporation. For subjects with higher forehead sweating rates, at least five sensors were necessary to calculate the evaporative sweat loss.

Adult↗
PubMed1995

The significance of sweat Cl/Na ratio in patients with borderline sweat test.

Recently a few cystic fibrosis (CF) patients with borderline or normal sweat tests have been reported. These patients present a diagnostic challenge. We aimed to study the sweat Cl/Na ratio in cystic fibrosis patients and to assess whether this ratio could be used as a diagnostic criteria. The mean sweat Cl/Na ratio of 3 groups was compared: Group A: 71 CF patients carrying 2 mutations known to be associated with severe disease presentation (delta F508, W1282X, G542X, N1303K, 1717-1G --> A). Group B: 10 compound heterozygous patients who carry one mutation associated with mild clinical disease (3849 + 10 kb --> T). Group C: 142 normal subjects. Sweat chloride levels higher than those of sodium were found in 96% of patients in Group A as compared to 3% of patients in Group C. In Group B 40% of the patients had sweat chloride levels higher than or equal to sodium levels. The mean Cl/Na ratio of Group A (1.2 +/- 0.1) differed significantly from that of Group B (0.94 +/- 0.1) and both groups had significant higher mean Cl/Na ratio compared to Group C (0.7 +/- 0.4) (P < 0.001). Thus in individuals with a borderline sweat test and a Cl/Na ratio > or = 1 the diagnosis of CF should be considered. However, a Cl/Na ratio < 1 does not exclude CF, since patients carrying mild mutations may have sweat sodium levels higher than those of chloride. Our findings suggest that the sweat Cl/Na ratio in CF is genetically determined and it may be of help in establishing the diagnosis of CF in patients with a borderline sweat test.

Child↗
PubMed1980

[Amino acid losses in human sweat. Influence of oral contraceptives, physical exercise and sex on the excretion of amino acids in sweat (author's transl)].

UNLABELLED: With the aid of ion exchange column chromatography we determined quantitatively the free amino acids in thermal sweat of the total human body surface. Sweat of 60 healthy men and 63 healthy women (aged 18-31 years) collected during 12 min of sauna bathing was investigated. Thirty men and 31 women were well trained, 33 women were taking oral, hormonal contraceptives. Sweat was deproteinised by adding an equal volume of 5% sulphosalicylic acid. RESULTS: 1. The comparison of the women taking oral contraceptives with the women not taking oral contraceptives showed no qualitative or significant quantitative differences in the excretion of amino acids in thermal sweat collected from the total body surface. 2. The comparison of the trained women with the untrained women neither revealed qualitative or significant quantitative differences in the excretion of amino acids in thermal sweat collected from the total body surface. 3. As compared to the trained men, untrained men excreted in thermal sweat collected from the total body surface significantly more alanine, arginine, citrulline, cystine, glycine, histidine, isoleucine, leucine, lysine, phenylalanine, serine, threonine, tyrosine, and valine. 4. The sex-specific comparison of the amino acid excretion in sweat showed that men had a significantly increased excretion of cystine, histidine, leucine, and taurine. Proline was detected only in the sweat of women. 5. The quantitative results obtained for the amino acid excretions during 12 min of sauna bathing suggest that persons exposed to hard, physical activity and/or high environmental temperatures have quite equal amino acid losses in sweat and in 24 h urine.

Adolescent↗
PubMed1999

Sweat production and localisation of carbonic anhydrase in the equine sweat gland during exercise at two ambient temperatures.

The aim of this investigation was to study sweat production during exercise at 2 ambient temperatures (20 degrees C and 35 degrees C) and the concurrent localisation of carbonic anhydrase (CA) in the sweat gland. Horses develop alkalosis during prolonged exercise and the sweat contains HCO3-. Carbonic anhydrase is therefore of interest since it catalyses the reaction CO2 + H2O<-->HCO3- + H+. Four standardbred trotters performed an exercise test. Skin biopsies were taken from the neck, and sweat rate, blood and skin temperatures were measured. There was a close relationship between sweat rate, temperatures and work intensity at 20 degrees C. Temperatures and sweat rate were higher at 35 degrees C and did not fall when the work intensity dropped. A significant decrease in the sweat gland cell area was found after exercise at 35 degrees C with an accompanying decrease of vesicles. Strong CA activity was present at the luminal cell membrane and weaker basolaterally. The staining intensity increased after exercise. We suggest that CA might be of importance for counteracting the alkalosis developed after exercise by delivering HCO3- for generation of the alkaline pH in sweat.

Animals↗
PubMed1984

Apparent absence of cystic fibrosis sweat factor on ion-selective and transport properties of the perfused human sweat duct.

Several previous studies have reported that a substance in exocrine products from cystic fibrosis (CF) patients is inhibitory to the transport of NaCl in several biological preparations. We have recently developed techniques for studying a target CF tissue, the eccrine sweat duct, and determined that salt absorption in the CF sweat duct appears to be decreased due to an impermeability to Cl. To determine whether this property might be induced, we have examined the sweat from patients with CF for potential influences on the ion-reabsorptive and ion-selective properties of sweat ducts from normal subjects. Isolated segments of sweat ducts from healthy volunteers were microperfused in vitro with concentration-adjusted sweat collected after thermal stimulation from CF patients and from normal subjects. The eccrine sweat duct may be best considered as a tight epithelium through which the mucosal uptake of NaCl proceeds via separate Na+ and Cl- pathways. As such, inhibitory actions of CF fluids should be exerted via an inhibition on one, or both, pathways, and should be expected to inhibit the electrolyte transport activity and alter the ion-selective properties of normal ductal tissue. We were unable to detect any effect of CF sweat on either property of the normal duct.

Adult↗
PubMed1994

Validity of the Wescor's sweat conductivity analyzer for the assessment of sweat electrolyte concentrations.

The purpose of this study was to compare the "NaCl equivalent" values determined by the Wescor's sweat conductivity analyzer (Sweat-Chek) with the sweat Na+ and Cl- concentration values measured by conventional methods. The sweat was induced by 60-min exercise and collected by a closed-pouch collector. The "NaCl equivalent" values determined by the sweat conductivity analyzer (mean: 75 mmol.L-1, range: 38 - 122, n = 72) were significantly (P < 0.05) greater than Na+ concentration values (mean: 71 mmol.L-1, range: 24 - 123, n = 72) measured by flame photometry and Cl-concentration values (mean: 61 mmol.L-1, range: 18 - 100, n = 48) measured by coulometric titration. The difference were most accentuated for low concentration values. The 95% confidence-agreement intervals around the mean differences between methods were 11 mmol.L-1 (14%) for both Na+ and Cl-. The Sweat-Chek conductivity analyzer is a portable instrument which approximates the actual Na+ and Cl- concentrations in sweat but with a positive bias probably due to the other unmeasured anions present in sweat.

Chlorides↗
PubMed2001

The clinical thermoregulatory sweat test induces maximal sweating.

Although thermoregulatory sweat testing is commonly used to assess the autonomic nervous system, the power of this stimulus to induce sweating has not been studied. In 8 healthy male subjects, the authors quantitated sweat rates, core temperature, heart rate, and blood pressure during clinical thermoregulatory sweat testing, a separate exercise protocol, and with exercise added to thermal conditions. The authors found that (1) the addition of exercise to the thermal environment produced no further increase in sweat rate (3,841+/-948 versus 3,888+/-866 nl/mn - cm2); (2) maximum sweat rates closely corresponded to the theoretical maximum (6,000 nl/mn - cm2) derived from single gland studies; (3) sweat rates vary across subjects, but are similar across sites in any one individual; (4) core temperature rise is a major determinant of cardiovascular load in both thermal and exercise settings; (5) blood pressure decreased 28/11 mm Hg during thermal load, but increased 26/10 mm Hg with exercise, in agreement with current understanding of muscle and skin vascular physiology. The authors conclude that clinical thermoregulatory testing conditions produce maximum sweat rates in humans.

Adolescent↗
PubMed1996

Clonidine increases the sweating threshold, but does not reduce the gain of sweating.

We tested the hypothesis that clonidine produces a dose-dependent increase in the sweating threshold but does not reduce the gain of sweating. Six healthy male volunteers were evaluated, each on three separate days in random order. In one, saline was administered; in another, a 2-micrograms/kg bolus of clonidine was followed by an infusion at 2 micrograms.kg-1.h-1, and on a third day, a 4-micrograms/kg bolus was followed by an infusion at 4 micrograms.kg-1.h-1. Core temperature was measured at the tympanic membrane and mean skin temperature was determined from four sites. A chest sweating rate of 40 g.m-2.h-1 was considered significant. The core temperature triggering sweating, adjusted to a designated mean skin temperature of 34 degrees C, identified the threshold for this response. Gain was defined by the adjusted core temperature increase required to augment sweating from 100 to 300 g.m-2.h-1. degree C-1. Plasma clonidine concentrations were 0.8 +/- 0.1 and 1.6 +/- 0.2 ng/mL on the small- and large-dose days, respectively. Clonidine administration increased the sweating threshold approximately 0.4 degree C (P < 0.05), but the increase was comparable at each dose. The gain of sweating was approximately 0.2 degree C and was not influenced by clonidine administration. The thermoregulatory effects of clonidine thus resemble those of volatile anesthetics, opioids, and propofol. These data suggest that the antishivering effect of clonidine results from central thermoregulatory inhibition rather than a specific peripheral action on thermogenic muscular activity. Unlike other sedatives and anesthetics, the concentration-dependence of clonidine demonstrates a ceiling beyond which the administration of an additional drug fails to enhance the effect, suggesting that the thermoregulatory effect of clonidine may be limited, even at high plasma concentrations. The gain of sweating was well preserved indicating that this response remains effective in the presence of sedatives and anesthetics.

Adrenergic alpha-Agonists↗
PubMed1985

The analysis of human sweat proteins by isoelectric focusing. I. Sweat collection utilizing the macroduct system demonstrates the presence of previously unrecognized sex-related proteins.

The presence of high concentrations of sodium in the sweat of patients with cystic fibrosis is widely accepted by all investigators as one of the most important manifestations of the genetic defect. However, the simple means of sweat collection utilized for diagnostic purposes has been extended to the biochemical and physical analysis of the macromolecular components of human sweat. The most popular technique for the attainment of sweat has been collection of sweat droplets from the skin surface following heat stimulation. In this report, it is demonstrated that a far superior means of sweat collection exists based on a new collection device called the MACRODUCT. Utilizing this device, in conjunction with thin-layer isoelectric focusing, demonstrated that human sweat contains sex-specific proteins expressed in adult males and absent or greatly decreased from females and prepubertal males. Additionally, results are presented which suggest that the presence of epidermal keratins are an excellent marker for sweat contaminated with nonsweat gland-derived macromolecules.

Adolescent↗
PubMed2006

The sweating foot: local differences in sweat secretion during exercise-induced hyperthermia.

INTRODUCTION: Little is known regarding local differences in foot sweat secretion. Since such information is important to our understanding of sweat gland control for thermoregulatory modeling and for the design of footwear we explored this topic. METHODS: Local sweat rates were investigated across core temperatures from 37-39 degrees C, achieved using endogenous (cycling) and exogenous heat (water-perfusion garment: 46 degrees C). Six healthy adults (three men, three women) performed one-legged, incremental cycling in a heated, climate-controlled chamber (36 degrees C, 60% relative humidity). Sweat rates were measured at the forehead and stationary (left) foot (capsules 3.16 cm2): three dorsal sites (base of toes, second metatarsal, and mid point), the lateral, and the central plantar surfaces. RESULTS: Terminal core temperatures ranged between 38.3-39.1 oC, with peak heart rates of 155-187 bpm. Most foot sweat rates were < 50% of that observed at the forehead: dorsal 1 (38%); dorsal 2 (54%); dorsal 3 (37%); lateral (24%); and plantar surfaces (18%). When averaged across the trial, local sweat rates were: 2.61 (forehead); 0.98 (dorsal 1); 1.39 (dorsal 2); 0.95 (dorsal 3); 0.62 (lateral); and 0.47 mg cm2 2 min-1 (plantar). CONCLUSION: Two key observations emerged. First, sweat secretion from the experimental foot averaged 30 ml x h(-1), peaking in the last 5 min at 50 ml x h(-1). Second, approximately 70% of the measured sweat flow emanated from the upper skin surfaces, with only 30% coming from the plantar surface.

Adult↗
PubMed1984

Sweat production in the isolated eccrine sweat gland of the rat.

A method has been developed to isolate a single rat eccrine sweat gland, together with the attached sweat duct, and to induce sweat secretion directly from the gland in vitro. Sweat production was induced using carbachol (2 X 10(-5) M to 3 X 10(-5) M) and methacholine (2 X 10(-5) M) in isolated plantar sweat glands maintained in a suitable environment (modified Krebs-Ringer bicarbonate at 38 degrees C containing 30% w/v fresh rat serum). The output of sweat was measured every 5 minutes for 85 minutes and the maximal final volume obtained with any one gland was 23 nl. Sweat production ceased on administration of appropriate concentrations of atropine (1 X 10(-5) M to 5 X 10(-5) M), withdrawal of calcium ions from the bathing fluid, and reduction of the medium temperature to 4 degrees C.

Animals↗
PubMed1984

Influence of calcium and cyclic nucleotides on beta-adrenergic sweat secretion in equine sweat glands.

The effects of Ca2+, the cyclic nucleotides adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP), and other parameters of sweat secretion from single equine sweat glands were examined in vitro. Extracellular Ca2+, the Ca2+ ionophore A23187, and the Ca2+ channel antagonist verapamil were all without effect on sweat secretion. Prolonged rinsing of the glands in Ca2+-free Ringer solution with 5 mM ethylenediaminetetraacetic acid decreased the secretion to 30% of the control sweat rate in response to the beta-adrenergic agonist isoproterenol; the sweat response was restored upon adding Ca2+ to the Ringer. cAMP but not cGMP analogues were as effective in stimulating sweat rates as isoproterenol, which elicited maximal secretory rates in vitro. cAMP stimulation was not inhibited by the beta-adrenergic antagonist propranolol. Because the equine sweat gland is predominantly stimulated via the beta-adrenergic receptor, we conclude that cAMP is a principal intracellular messenger in coupling this type of stimulus to the fluid secretion response in this tissue.

Animals↗