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PubMed2001

Associated change in plantar temperature and sweating after transthoracic endoscopic T2-3 sympathectomy for palmar hyperhidrosis.

OBJECT: Transthoracic endoscopic T2-3 sympathectomy is currently the treatment of choice for palmar hyperhidrosis. Compensatory sweating of the face, trunk, thigh, and sole of the foot was found in more than 50% of patients who underwent this procedure. The authors conducted this study to investigate the associated intraoperative changes in plantar skin temperature and postoperative plantar sweating. METHODS: One hundred patients with palmar hyperhidrosis underwent bilateral transthoracic endoscopic T2-3 sympathectomy. There were 60 female and 40 male patients who ranged in age from 13 to 40 years (mean age 21.6 years). Characteristics studied included changes in palmar and plantar skin temperature measured intraoperatively, as well as pre- and postoperative changes in plantar sweating and sympathetic skin responses (SSRs). In 59 patients (59%) elevation of plantar temperature was demonstrated at the end of the surgical procedure. In this group, plantar sweating was found to be exacerbated in three patients (5%); plantar sweating was improved in 52 patients (88.1%); and no change was demonstrated in four patients (6.8%). In the other group of patients in whom no temperature change occurred, increased plantar sweating was demonstrated in three patients (7.3%); plantar sweating was improved in 20 patients (48.8%); and no change was shown in 18 patients (43.9%). The difference between temperature and sweating change was significant (p = 0.001). Compared with the presympathectomy rate, the rate of absent SSR also significantly increased after sympathectomy: from 20 to 76% after electrical stimulation and 36 to 64% after deep inspiration stimulation, respectively (p < 0.05). CONCLUSIONS: In contrast to compensatory sweating in other parts of the body after T2-3 sympathetomy, improvement: in plantar sweating was shown in 72% and worsened symptoms in 6% of patients. The intraoperative plantar skin temperature change and perioperative SSR demonstrated a correlation between these changes.

Adolescent↗

PubMed2005

Deficiency of dermcidin-derived antimicrobial peptides in sweat of patients with atopic dermatitis correlates with an impaired innate defense of human skin in vivo.

Antimicrobial peptides are an integral part of the epithelial innate defense system. Dermcidin (DCD) is a recently discovered antimicrobial peptide with a broad spectrum of activity. It is constitutively expressed in human eccrine sweat glands and secreted into sweat. Patients with atopic dermatitis (AD) have recurrent bacterial or viral skin infections and pronounced colonization with Staphylococcus aureus. We hypothesized that patients with AD have a reduced amount of DCD peptides in sweat contributing to the compromised constitutive innate skin defense. Therefore, we performed semiquantitative and quantitative analyses of DCD peptides in sweat of AD patients and healthy subjects using surface-enhanced laser desorption ionization time-of-flight mass spectrometry and ELISA. The data indicate that the amount of several DCD-derived peptides in sweat of patients with AD is significantly reduced. Furthermore, compared with atopic patients without previous infectious complications, AD patients with a history of bacterial and viral skin infections were found to have significantly less DCD-1 and DCD-1L in their sweat. To analyze whether the reduced amount of DCD in sweat of AD patients correlates with a decreased innate defense, we determined the antimicrobial activity of sweat in vivo. We showed that in healthy subjects, sweating leads to a reduction of viable bacteria on the skin surface, but this does not occur in patients with AD. These data indicate that reduced expression of DCD in sweat of patients with AD may contribute to the high susceptibility of these patients to skin infections and altered skin colonization.

Adult↗

PubMed1994

Autonomic nerve dysfunction in COPD as assessed by the acetylcholine sweat-spot test.

Patients with hypoxic chronic obstructive pulmonary disease (COPD) have evidence of a subclinical parasympathetic autonomic neuropathy, with apparent preservation of sympathetic function. However, these cardiovascular-respiratory tests might have been biased by concomitant chest disease, the acetylcholine sweat-spot test avoids this bias. This sweat-spot test assesses sympathetic nerve function, it relies upon the fact that denervated sweat glands do not produce sweat. 35 patients with hypoxaemic COPD and seven age matched normal subjects were studied. Following intradermal injection of 0.1 of 1% acetylcholine into the dorsum of the feet, the number of sweatglands able to respond in a given surface area was recorded. Cardiovascular autonomic nerve function, arterial oxygen and carbon dioxide tensions, lung function and cigarette consumption were also recorded. The acetylcholine sweat-spot test was highly repeatable in eight COPD patients, no person with normal or frankly abnormal function being wrongly assigned. The age matched control subjects had normal acetylcholine sweat-spot scores and cardiovascular autonomic tests. The acetylcholine sweat-spot test was abnormal in 24 patients, borderline in 8 and normal in 3 patients. The abnormal sweat-spot test group had significant worse FEV1, arterial blood gases and autonomic function. The acetylcholine sweat-spot score correlated with the severity of arterial hypoxaemia (r = 0.78, p < 0.001) and with the parasympathetic cardiovascular tests (r = 0.80, p < 0.001). In conclusion, patients with hypoxaemic COPD have a parasympathetic cardiovascular and a peripheral sympathetic autonomic neuropathy. The acetylcholine sweat-spot test is repeatable, easy to perform and a sensitive indicator for autonomic dysfunction in breathless individuals with COPD.

Acetylcholine↗

PubMed1996

Sweat chloride concentrations in infants homozygous or heterozygous for F508 cystic fibrosis.

OBJECTIVE: To determine whether an adequate volume of sweat could be obtained routinely from infants younger than 6 weeks old and to evaluate sweat chloride levels in infants with known genotype statuses, including heterozygote carriers for cystic fibrosis (CF). METHODOLOGY: Infants were evaluated using pilocarpine iontophoresis and measurement of sweat volume and chloride concentration. The majority of these infants were referred because of newborn screening test results positive for CF based on immunoreactive trypsinogen analysis. DNA analyses for the 3-base pair deletion at codon 508 of the CF transmembrane regulator gene (F508 mutation) were performed whenever possible, and patients with CF were categorized by genotype. RESULTS: Sweat tests were performed successfully (>/-50 mg of sweat) in 99.3% of the infants tested, and there was no difference in the proportion of unsuccessful tests in infants younger than or older than 6 weeks of age. The normal mean +/- SD sweat chloride was 10.6 +/- 5.2 mEq/L (95% confidence interval, 9.9-11.3). Patients with CF who are F508 homozygotes or F508 compound heterozygotes or who have two other non-F508 mutant alleles were shown to have similar sweat chloride levels, with mean values of 99.9, 98.8, and 96.6 mEq/L, respectively. The group of infants who were found to be CF (F508) heterozygote carriers, when compared with the healthy group, had mildly but significantly increased sweat chloride concentrations, with a mean +/- SD of 14.9 +/- 8.4 mEq/L (95% confidence interval, 13.4-16.4). CONCLUSIONS: Quantitative pilocarpine iontophoresis can be used successfully in infants younger than 6 weeks of age who are undergoing routine diagnostic evaluations to follow up newborn screening test results that are positive for CF. The upper limit of normal sweat chloride in infants should be revised to 40 mEq/L (mean + 3 SD of the CF heterozygote carrier group). CF heterozygote carrier infants with one F508 mutant allele show phenotypic manifestations of CF, including subclinical elevations of sweat chloride.

Age Factors↗

PubMed1994

Secretion of ions and pharmacological responsiveness in the mouse paw sweat gland.

1. Some of the basic functional features of the mouse paw eccrine sweat gland were delineated to allow comparison with those of transgenic mice in the future. 2. The mouse sweat secretory coil responds to methacholine, elaborating a K(+)-rich (> 120 mmol/l), Na(+)-poor (< 70 mmol/l) primary fluid as does the rat paw sweat gland, as previously reported. The methacholine-induced sweat rate increases with age in parallel with the growth of the sweat gland over the first 6 weeks of life. 3. The sweating response to cyclic AMP-elevating agents, such as isoprenaline or forskolin, is as much as 40% of the methacholine-induced sweat rate at 1 week of age, but falls to 10% by 6 weeks of age despite the fact that the agonist-induced tissue accumulation of cyclic AMP expressed on a per microgram of protein basis triples with age over the same period. 4. A marked K+ outflux was also noted in response to methacholine and a small K+ outflux was seen in response to cyclic AMP-elevating agonists in superfused adult mouse secretory coils in vitro. 5. Since sweat secretion is usually associated with activation of either K+ channels or Cl- channels or both, and since the sweating occurred in response to cyclic AMP-elevating agonists, we speculate that the cyclic AMP-activated Cl- channels (the mouse version of the cystic fibrosis transmembrane conductance regulator) may also occur in the mouse sweat gland, but that the degree of their expression may be influenced by the age of the mice.

Aging↗

PubMed2001

Immunohistochemical localization of activated EGF receptor in human eccrine and apocrine sweat glands.

Epidermal growth factor (EGF) is secreted into sweat from secretory cells of human sweat glands. The function of EGF in sweat is poorly understood. The biological function of EGF is exerted by the binding of EGF to the receptor (EGFR) and its activation. Therefore, we immunohistochemically localized the activated form of EGFR in human eccrine and apocrine sweat glands to assess the functional importance of the EGF-EGFR system in human sweat glands. Frozen sections of human skin were stained with a monoclonal antibody (MAb) specific for tyrosine-phosphorylated (activated) EGFR and with an MAb that stains both activated and non-activated EGFR. In the secretory portion of eccrine sweat glands, nuclei of the secretory cells were stained with the anti-activated EGFR MAb. In coiled and straight portions of eccrine sweat ducts, nuclei of luminal and peripheral cells were stained with the antibody specific for activated EGFR. Luminal cell membranes and luminal cytoplasm of inner ductal cells possessed non-activated EGFR. In the secretory portion of apocrine sweat glands, activated EGFRs were present in cytoplasm and nuclei of secretory cells. These data suggest that EGF, already known to be present in the cytoplasm of secretory cells in eccrine and apocrine sweat glands, activates EGFR in the nuclei of secretory cells themselves in an intracrine manner. Because ductal cells do not express EGF, EGF in the sweat secreted from the secretory cells should activate EGFR in the ductal cells in a paracrine manner. (J Histochem Cytochem 49:597-601, 2001)

Antibodies, Monoclonal↗

PubMed2004

3-Methyl-3-sulfanylhexan-1-ol as a major descriptor for the human axilla-sweat odour profile.

This study sets out to redress the lack of knowledge in the area of volatile sulfur compounds (VSCs) in axillary sweat malodour. Sterile odourless underarm sweat (500 ml) was collected from 30 male volunteers after excessive sweating. Five strains of bacteria, Corynebacterium tuberculostearicum, Corynebacterium minutissimum, Staphylococcus epidermidis, Staphylococcus haemolyticus, and Bacillus licheniformis, were isolated and characterised for their ability to generate an authentic axillary odour from the sweat material collected. As expected, all of the five bacterial strains produced strong sweat odours. Surprisingly, after extensive olfactive evaluation, the strain of Staphylococcus haemolyticus produced the most sulfury sweat character. This strain was then chosen as the change agent for the 500 ml of odourless underarm sweat collected. After bacterial incubation, the 500-ml sample was further processed for GC-olfactometry (GC-O), GC/MS analysis. GC-O of an extract free of organic acids provided three zones of interest. The first was chicken-sulfury, the second zone was onion-like, and the third zone was sweat, clary sage-like. From the third zone, a new impact molecule, (R)- or (S)-3-methyl-3-sulfanylhexan-1-ol, was isolated and identified by GC/MS, MD-GC, and GC AED (atomic emission detector). (S)-3-methyl-3-sulfanylhexan-1-ol was sniff-evaluated upon elution from a chiral GC column and was described as sweat and onion-like; its opposite enantiomer, (R)-3-methyl-3-sulfanylhexan-1-ol, was described as fruity and grapefruit-like. The (S)-form was found to be the major enantiomer (75%).

Adult↗

PubMed1975

[Free amino acids in human Eocrine sweat (author's transl)].

With the aid of ion exchange column chromatography we determined quantitatively the free amino acids in eccrine, thermal sweat. Sweat was collected (a) from the face of 27 healthy men and 26 healthy women (b) from the face, chest, armpits, shoulders, back, upper part of the abdomen, hypogastrium, forearms and thighs of the same individual and (c) from the face of the same individual at different times. Sweat was deproteinised by adding an equal volume of 5% sulphosalicylic acid. 1. The results showed not only a constant, qualitative amino acid pattern in sweat, but also a relative constancy among the individual amino acids. 2. The concentrations of the free amino acids in sweat showed significant, individual variations. Particularly high excretion rates were observed in the following amino acids: alanine, glycine, citrulline, histidine, ornithine, threonine and serine. 3. As compared to men, women had an increased excretion of all the examined amino acids in sweat from the face, except for cystine. Statistically significant higher excretion was seen within this sex-specific comparison for the following amino acids: alanine, citrulline, glycine, histidine, isoleucine, serine, taurine, threonine, tyrosine and valine. 4. Essential amino acids such as isoleucine, leucine, lysine, methionine, phenylalanine and valine and also cystine were always excreted only in small amounts. 5. Significant differences were also observed in the total amino acid excretion and in the individual amino acid excretions in sweat obtained from different parts of the body of the same person. 6. The amino acid concentrations determined in the sweat from the face of the same individual at different times showed a relative constancy as compared to the large differences of the amino acid concentrations determined in the sweat from the face of different individuals.

Amino Acids↗

PubMed1998

[Sex-dependent differences in sweating of normal probands and atopic patients in cardiovascular stress].

Sweating (perspiratio sensibillis) due to cholinergic sweat gland activity serves predominantly for thermoregulation and is triggered among others by physical stress. Individuals suffering from atopic eczema usually respond to sweating with generalized itching. Different sweat regulation in atopic patients and healthy controls under cholinergic stimulation and heat chamber provocation tests has already been examined in several studies. However, no clinical trial has yet been done on atopic sweat regulation during physical stress. Sex-specific sweat secretion rates have not been evaluated. In our trial we compared sweat amounts of male and female atopics (14 m, 10 f) and healthy controls (14 m, 10 f) during and after physical activity on a bicycle ergometer. We used a special sweat collector system reliable even at intensive body movement. The individual stress limit had been determined by previous endurance training with lactate level and heart rate measurement. We found a highly significant difference in maximum sweat amounts between atopics and controls. On average, healthy individuals (of both sexes) perspired nearly three times as much as atopic patients. Male controls perspired nearly twice as much as corresponding females. Among the atopics, sex-specific differences were found to be not statistically relevant.

Adolescent↗

PubMed2006

Genomic and non-genomic effects of aldosterone on the individual variation of the sweat Na+ concentration during exercise in trained athletes.

To clarify whether the resting background effects (genomic) or exercise-related action (non-genomic) of aldosterone (ALD) is primarily affected to an individual variation in the sweat Na+ concentration ([Na+]sweat), we analyzed the cross-sectional relationship between [Na+]sweat and the plasma ALD concentration during rest and exercise in a hot environment. Eleven college-aged male subjects with a mean maximal oxygen uptake of 48 (range 42-59) ml kg-1 min-1 performed three sessions of 20-min cycle exercise at two levels of intensity (40 or 60% VO2max) in a room maintained at 31 degrees C. The chest sweat rate (SRch) and its containing Na+ were higher and individual differences in SRch and [Na+]sweat were greater at 60% exercise than at 40% exercise. In each individual, the [Na+]sweat increased significantly (P<0.05) with the increase in the SRch. In all subjects, the mean [Na+]sweat during exercise correlated negatively with the resting plasma ALD level at either percentage, but it did not correlate with the exercising ALD. These results suggest that individual variations in the increase of the [Na+]sweat in response to a rise in the SRch may thus be more closely related to the resting ALD than to the exercising ALD. As a result, the genomic action of ALD may be affected more by the sweat Na+ variation than by the rapidly non-genomic action during exercise in humans.

Adult↗

PubMed2004

Sweat lactate response during cycling at 30 degrees C and 18 degrees C WBGT.

Sweat lactate reflects eccrine gland metabolism. However, the metabolic tendencies of eccrine glands in a hot versus thermoneutral environment are not well understood. Sixteen male volunteers completed a maximal cycling trial and two 60-min cycling trials [30 degrees C = 30 +/- 1 degrees C and 18 degrees C = 18 +/- 1 degrees C wet bulb globe temperature (WBGT)]. The participants were requested to maintain a cadence of 60 rev min(-1) with the intensity individualized at approximately 90% of the ventilatory threshold. Sweat samples at 10, 20, 30, 40, 50 and 60 min were analysed for lactate concentration. Sweat rate at 30 degrees C (1380 +/- 325 ml x h(-1)) was significantly greater (P < 0.05) than at 18 degrees C (632 +/- 311 ml x h(-1)). Sweat lactate concentration was significantly greater (P < 0.05) at each time point during the 18 degrees C trial, with values between trials tending to converge across time. During the 30 degrees C trial, both heart rate (20, 30, 40, 50 and 60 min) and rectal temperature (30, 40, 50 and 60 min) were significantly higher than in the 18 degrees C trial. Higher sweat lactate concentrations coupled with lower sweat rates may indicate a greater relative contribution of oxygen-independent metabolism within eccrine glands during exercise at 18 degrees C. Decreases in sweat lactate concentration across time suggest either greater dilution due to greater sweat volume or increased reliance on aerobic metabolism within eccrine glands. The convergence of lactate concentrations between trials may indicate that time-dependent modifications in sweat gland metabolism occur at different rates contingent partially on environmental conditions.

Adult↗

PubMed1987

Effect of periglandular ionic composition and transport inhibitors on rhesus monkey eccrine sweat gland function in vitro.

1. The effects of peritubular ions and transport inhibitors were studied on methacholine (MCH)-induced sweat secretion by the isolated, cannulated monkey palm sweat glands in vitro and on the transepithelial and basolateral membrane potential (p.d.). 2. Sweat secretory rate was a curvilinear function of peritubular Na+ and Cl- concentration. Among the anion substitutes only Br- was able to totally substitute for Cl-. Presence of HCO3- or H2PO4- in the bath was not essential. 3. Both bumetanide and furosemide inhibited sweat secretion in a dose-dependent manner with the median effective concentration (EC50) of 3 X 10(-6) and 3 X 10(-5) M, respectively. 4. Bumetanide (10(-4) M) had no significant effect on basolateral membrane p.d. but nearly abolished the transepithelial p.d. 5. Hydrochlorothiazide (HCTZ, 3 X 10(-4) M) inhibited sweat secretion by only 35%. Inhibitors of ion exchangers amiloride (10(-4) M) and DIDS (4,4'-diisothiocyanostilbene-2,2'-disulphonic acid, 10(-4) M) lowered sweat secretion by less than 20%. 6. Removal of peritubular K+ as well as addition of 5 mM-Ba2+ also inhibited sweat rate. 5 mM-Ba2+ abolished the transepithelial p.d. and depolarized the basolateral p.d. by 26 mV, although the effects of Ba2+ on sweating and the transepithelial p.d. were only transient. 7. The data raise a possibility that either the NaCl or Na+-K+-2Cl- co-transport system or both may be involved in MCH-induced sweat secretion, whereas the role of parallel ion exchangers, if any, may be rather minor.

Action Potentials↗

PubMed2005

Sweat and sodium losses in NCAA football players: a precursor to heat cramps?

This observational study was designed to determine whether football players with a history of heat cramps have elevated fluid and sodium losses during training. During a "two-a-day" training camp, five Division I collegiate football players (20.2 +/- 1.6 y, 113 +/- 20 kg) with history of heat cramps (C) were matched (weight, age, race and position) with a cohort of teammates (19.6 +/- 0.6 y, 110 +/- 20 kg) who had never cramped (NC). Change in body weight (adjusted by fluid intake) determined gross sweat loss. Sweat samples (forearm patch) were analyzed for sodium and potassium concentrations. Ad libitum fluid intake was measured by recording pre- and post-practice bottle weights. Average sweat sodium loss for a 2.5-h practice was projected at 5.1 +/- 2.3 g (C) vs. 2.2 +/- 1.7 g (NC). When averaged across two practices within the day, fluid intake was similar between groups (C: 2.6 +/- 0.8 L vs. NC: 2.8 +/- 0.7 L), as was gross sweat loss (C: 4.0 +/- 1.1 L vs. NC: 3.5 +/- 1.6 L). There was wide variability in the fluid deficit incurred for both C and NC (1.3 +/- 0.9 vs. 0.7 +/- 1.2%) due to fluid intake. Sweat potassium was similar between groups, but sweat sodium was two times higher in C versus NC (54.6 +/- 16.2 vs. 25.3 +/- 10.0 mmol/L). These data indicate that sweat sodium losses were comparatively larger in cramp-prone football players than in NC. Although both groups consumed sodium-containing fluids (on-field) and food (off-field), both appeared to experience an acute sodium deficit at the end of practices based on sweat sodium losses. Large acute sodium and fluid losses (in sweat) may be characteristic of football players with a history of heat cramping.

Adult↗

PubMed1979

Human skin wettedness and evaporative efficiency of sweating.

Rates of evaporation and sweating were recorded for three acclimatized male subjects in hot humid conditions, the ambient parameters of which were set so that the various imposed evaporative rates required the same skin wettedness at different levels of sweating. Rectal and skin temperatures were measured. Results showed that during steady state occurring during the 2nd h of exposure each subject reached the required evaporative rate by means of increases in skin wettedness regardless of the level of sweating; the sweat evaporative efficiency, defined as the ratio between evaporative rate and sweat rate, decreased as skin wettedness increased, in a range between 0.74 and 1.0 Sweat efficiency fell to 0.67 for fully wet skin. The body temperatures did not increase with time if skin wettedness was less than unity. Evaporative heat transfer coefficient (he), maximum evaporative capacity, and wettedness were estimated on the basis of the observed decrease of sweat efficiency. The relationship between skin wettedness and sweat efficiency was interpreted as a combined effect of differences in local he as well as in local sweat rates.

Adult↗

PubMed1983

Composition of sweat of the horse during prolonged epinephrine (adrenaline) infusion, heat exposure, and exercise.

Temporal changes in sweat composition were studied in 4 horses during epinephrine (adrenaline) infusion (0.13 to 0.31 micrograms/kg/min for 3 hours), heat exposure (41 C, [33 C wet bulb] for 5 to 6 hours), and exercise (16 to 18 km/hr for 58 to 80 km). Four ponies also were studied during heat exposure. Sweat produced by each of the stimuli was hypertonic for Na+, K+, and Cl-. These electrolyte concentrations remained constant during the central period of the experiments, with changes occurring near the beginning and toward the end. The Na+ was significantly higher and K+ significantly lower in epinephrine-induced sweat than in heat-induced sweat, and the pattern of change in sweat Na/K ratio varied among the 3 stimuli. The Ca2+ concentration decreased with time and was hypotonic after 15 minutes of epinephrine-induced sweating. Concentrations of Mg2+ and protein decreased exponentially with time. There was a high correlation between them, although the Mg2+ was not protein-bound. Sweat urea concentration was directly related to plasma urea concentration. When plasma glucose concentration became greater than 10 to 12 mmole/L during epinephrine infusion, glucose appeared in the sweat and its concentration rose to 8 to 12 mmole/L of sweat when plasma glucose was more than 20 mmole/L.

Animals↗

PubMed1985

Dynamics of sweating in men and women during passive heating.

The dynamics of sweating was investigated at rest in 8 men and 8 women. Electrical skin resistance (ESR), rectal temperature (Tre) and mean skin temperature (Tsk) were measured in subjects exposed to 40 degrees C environmental temperature, 30% relative air humidity, and 1 m X s-1 air flow. Sweat rate was computed from continuous measurement of the whole body weight loss. It was found that increases in Tre, Tsk and mean body temperature (Tb) were higher in women than in men by 0.16, 0.38 and 0.21 degrees C, but only the difference in delta Tb was significant (p less than 0.05). The dynamics of sweating in men and women respectively, was as follows: delay (td) 7.8 and 18.1 min (p less than 0.01), time constant (tau) 7.5 and 8.8 min (N.S.), inertia time (ti) 15.3 and 26.9 min (p less than 0.002), and total body weight loss 153 and 111 g X m-2 X h-1 (p less than 0.001). Dynamic parameters of ESR did not differ significantly between men and women. Inertia times of ESR and sweat rate correlated in men (r = 0.93, p less than 0.001), and in women (r = 0.76, p less than 0.02). In men, delta Tre correlated with inertia time of sweat rate (r = 0.81, p less than 0.01) as well as with the inertia time of ESR (r = 0.83, p less than 0.001). No relation was found between delta Tre and the dynamics of sweating in women. It is concluded that the dynamics of sweating plays a decisive role in limiting delta Tre in men under dry heat exposure. The later onset of sweating in women does not influence the rectal temperature increase significantly. In women, delta Tre is probably limited by a complex interaction of sweating, skin blood flow increase, and metabolic rate decrease.

Adult↗

PubMed1995

Cutaneous vasodilatation responses synchronize with sweat expulsions.

To examine whether cutaneous active vasodilatation is mediated by sudomotor nerve fibres we recorded cutaneous blood flow and sweat rates continuously with laser-Doppler flowmetry and capacitance hygrometry, respectively, from the dorsal and plantar aspects of the foot in 11 male subjects at varying ambient temperatures (Ta) between 22 and 40 degrees C (relative humidity 40%). In a warmer environment (Ta 29-40 degrees C), predominant responses of the blood flow curve from the sole of the foot were transient depressions (negative blood flow responses, NBR), whereas those from the dorsal foot were transient increases (positive blood flow responses, PBR). The PBR on the dorsal foot occurred spontaneously or in response to mental or sensory stimuli, and when PBR did not fuse with each other the rate of PBR was linearly related to tympanic temperature. When dorsal foot sweating was continuous, PBR on the dorsal foot almost entirely synchronized with sweat expulsion. When dorsal foot sweating was intermittent PBR sometimes occurred on the dorsal foot without corresponding sweat expulsions, but these PBR showed a complete correspondence with subthreshold sweat expulsion seen on a methacholine-treated area. The amplitude and the duration of PBR showed a significant linear relationship with the amplitude and the duration of the corresponding sweat expulsion. In a thermoneutral or cooler environment (Ta 22-29 degrees C), PBR occurred on the sole of the foot when mental or sensory stimuli elicited sweating in that area. Thus, PBR occurred when and where sweating appeared. Atropine failed to abolish PBR on the dorsal foot. Blockade of the peroneal nerve eliminated both PBR and NBR on the dorsal foot.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Plasma ammonia is the principal source of ammonia in sweat.

Sweat contains ammonia. However, neither its source nor factors affecting its concentration in the sweat are known. The aim of this study was to examine the effect of plasma concentrations of ammonia and urea on the concentration of ammonia in the sweat. Four groups of male volunteers were examined: one control, two after ingestion of ammonium chloride, three cirrhotic, hyperammonaemic, four uraemic. Sweat was collected from each subject from the palmar side of the forearm using gauze pads, after previous iontophoresis of pilocarpine. Ammonia and urea concentrations were determined in the sweat and in the plasma. It was found that elevated plasma ammonia concentration in healthy subjects after ingestion of ammonium chloride as well in the cirrhotic patients resulted in an increase of ammonia concentration in the sweat. High plasma and sweat urea concentration in the uraemic subjects did not affect the concentration of ammonia in the sweat. It was concluded that plasma ammonia was the principal source of ammonia in the sweat.

Administration, Oral↗