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PubMed1968

The effects of soaking the skin in water at various temperatures on the subsequent ability to sweat.

1. The ability of two human subjects to produce sweat was measured before and after immersion for up to 4 hr in water at 32-36 degrees C (soak).2. The ability to produce sweat declined about 4 times as rapidly when the subject was soaked at 36 degrees C as at 32 degrees C.3. The rate of decline characteristic of soaking at 36 degrees C was shown by subjects exercising in water at 35 degrees C, but not at rest at 35 degrees C. The difference appeared to be related to the presence or absence of moderate sweating (300 g/hr) during the soak. At higher rates there was no further increase in the rate of decline.4. Soaking at 39 degrees C for 5 min, after which the water temperature was reduced to 33 degrees C, caused a decline consistent with the supposition that while the subject was sweating the rate of decline was the same as that at 36 degrees C and for the rest of the time the same as that at 32 degrees C.5. It is concluded that the rate of decline is increased if the sweat ducts are perfused, and some possible mechanisms are discussed.

Body Weight↗

PubMed1987

Partial purification and characterization of cysteine proteinases in eccrine sweat.

Attempts were made to purify and characterize cysteine proteinases in human eccrine sweat and further clarify their origin. Benzoyl-DL-arginine-beta-naphthylamide (BANA) and L-leucine beta-naphthylamide (LeuNA) hydrolases in thermally induced sweat were sequentially purified by Sephacryl S-200 chromatography and chromatofocusing, which yielded two major peaks of BANA hydrolase activity, BANA-I and BANA-II. Both enzymes are cysteine proteinases as evidenced by stimulation of enzymic activity by dithiothreitol and ethylenediaminetetraacetic acid and its inhibition by iodoacetic acid, (PCMB), and trans-epoxysuccinyl-L-leucylamido-(4-guanidino)-butane (E-64). Unlike BANA-II, BANA-I showed an additional aminopeptidase activity, an affinity to concanavalin A-Sepharose but no affinity to organomercurial sepharose and failed to hydrolyze benzyloxycarbonyl-phenylalanyl-arginine 4-methyl 7-coumarylamide (Z-Phe-Arg-NMec), a specific substrate for cathepsin B, which is poorly sensitive to leupeptin [inhibitor constant (Ki) = 1 X 10(-5) M] and relatively heat resistant. These and other characteristics such as its isoelectric points (PI) (= 5.8) and the Km for Arg-NMec (0.1 mM) and BANA (0.71 mM) all support the possibility that BANA-I is closely related to cathepsin H. In contrast, BANA-II is sensitive to Zn2+, leupeptin (Ki = 5.5 X 10(-9) M), is not adsorbed by concanavalin A- (Con-A)Sepharose, but is bound to organomercurial sepharose. It has a specificity to Z-Phe-Arg-NMec but not to Arg-NMec, has the molecular weight of 27, PI of 5.2, the pH optima for BANA (6.0), and the Km for BANA of 3.3 mM and the Km for Z-Phe-Arg-NMec of 0.1 mM. These features resemble those of liver cathepsin B. Leupeptin-sensitive BANA hydrolase was observed in the glandular extract of isolated sweat glands, which was increased after stimulation with methacholine and isoproterenol in vitro. The data are consistent with the notion that cathepsins B- and H-like enzymes are present in eccrine sweat and the former may be derived from the sweat gland.

Benzoylarginine-2-Naphthylamide↗

PubMed1978

High concentration of sweat calcium, magnesium and phosphate in chronic renal failure.

Sweat collected from the forearm of chronic renal failure and control patients, after iontophoretic stimulation with pilocarpine, was analyzed for Na, K, Cl, Mg, phosphate and urea. Concentrations of Ca, Mg and phosphate in sweat from chronic renal failure patients were significantly elevated (p less than 0.05) as compared to controls, while the concentrations of Na, K, and Cl were normal. The mean sweat rates and apparent skin conductivities were lower in uremics, but not significantly different from controls (0.05 less than p less than 0.10). Tentatively it is concluded that the increase of Ca, Mg and phosphate in uremic sweat is due to an increase in the secretion of these electrolytes in the secretory portion of the sweat gland, while the reabsorptive duct is normal.

Calcium↗

PubMed1993

Decreased sweating in seven patients with Laron syndrome.

Previous studies have shown that sweat secretion was reduced in patients with GH deficiency and increased during GH treatment, indicating an influence of GH on sweat gland function. Thus, patients with GH deficiency have impaired thermoregulation. We report on sweat secretion rates (SSRs) in seven patients with Laron syndrome, measured by pilocarpine iontophoresis. The patients had significantly lower SSRs than healthy children matched for sex and pubertal stage (P < 0.00005) and moderately, but significantly, elevated sweat electrolyte concentrations (P < 0.00005 for potassium; P < 0.01 for sodium). These observations further supported the hypothesis that sweat gland function in humans is under the influence of the GH-insulin-like growth factor-I axis. It remains to be seen whether the decrease in SSR also leads to altered thermoregulation in patients with Laron syndrome.

Adolescent↗

PubMed1986

Quantitative analysis of the local effect of skin temperature on sweating.

Effects of local skin temperature on sweat gland activity were analyzed quantitatively by measuring changes in the rates of thermal sweating and of drug-induced sweating by local heating. The data indicates that a rise in local temperature causes an accelerated increase in the rate of sweat production, the Q10 being around 2.5 regardless of the basal sweat rate with some individual variations. Local heating apparently facilitates transmitter release at the neuroglandular junction and augments glandular responsiveness, their significances being comparable.

Adult↗

PubMed1992

Sweat gland response to exercise in the heat among pre-, mid-, and late-pubertal boys.

Sweating rate (SR) of boys is lower than that of men. To assess the association between the response of individual sweat glands and physical growth and maturation, three groups of circumpubertal boys cycled at 50% VO2max in a climatic chamber (42 degrees C, 20% relative humidity). Based on Tanner staging (pubic hair), 16 were classified as prepubertal (PP, Tanner 1), 15 as midpubertal (MP, Tanner 2-4), and five as late-pubertal (LP, Tanner 5). Population density (PD) of the heat-activated sweat glands, the mean area of sweat drops (DA), and the proportion of skin covered by sweat (%A) were measured by skin photography and computer-assisted imaging analysis. Other measurements included rectal and skin temperatures (Tre, Tsk, respectively), heart rate (HR), and total body SR. The rise in HR, Tre and Tsk did not differ among groups. Whole body SR was significantly higher in the LP group compared with PP (PP = 4.95 +/- 0.23, MP = 5.79 +/- 0.20, LP = 6.70 +/- 0.42 ml.min-1.m-2) (mean +/- SEM). PD was significantly higher in the PP group (PP = 128 +/- 8, MP = 97 +/- 9, LP = 74 +/- 9 glands.cm-2), while DA was higher in the LP group (PP = 5.47 +/- 0.59, MP = 6.92 +/- 0.47, LP = 12.83 +/- 1.41 microns2.10(4)). %A did not differ among groups. The calculated SR per gland was higher among the LP groups compared with the less mature ones (PP = 4.6 +/- 0.3, MP = 7.2 +/- 0.8, LP = 9.6 +/- 1.0 nl.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

[Sweat-gland function in patients with X-linked ichthyosis].

Literature reports that patients affected by X-linked ichthyosis (XLI) have a reduction of sweat glands and a decrease of sweat production. The sweat physiology of 28 patients, 14 with XLI, 7 with lamellar ichthyosis, 7 with dominant ichthyosis and 28 control subjects were examined with sweat test, performed by pilocarpine iontophoresis. In the same patients we have performed skin biopsy to evaluate quantitative and qualitative reduction of sweat glands.

Adolescent↗

PubMed1986

Sweat bromide excretion in cystic fibrosis.

Sweat reabsorption of bromide and chloride was studied in controls, obligate carriers of the cystic fibrosis gene, and individuals with cystic fibrosis. Sweat and serum ultrafiltrate concentrations of bromide and chloride were determined by an anion-exchange chromatographic method. The reabsorption of each ion was determined by the ratio of the sweat concentration to the serum ultrafiltrate concentration. Sweat bromide reabsorption paralleled chloride reabsorption in each of the groups. The mean bromide reabsorption ratio for 12 controls was 0.10 +/- 0.10 (range 0 to 0.26), for 11 obligate carriers 0.09 +/- 0.09 (range 0 to 0.24), and for 13 individuals with cystic fibrosis 0.86 +/- 0.26 (range 0.47 to 1.38). The mean chloride reabsorption ratio for the controls was 0.24 +/- 0.11 (range 0.06 to 0.45), for the obligate carriers 0.22 +/- 0.10 (range 0.10 to 0.45), and for individuals with cystic fibrosis 0.95 +/- 0.09 (range 0.76 to 1.1). Thus, there was a significant decrease in bromide reabsorption in individuals with cystic fibrosis compared with controls (P less than 0.001) and heterozygotes (P less than 0.001), which was similar for chloride. As with chloride reabsorption, no difference was found in bromide reabsorption between obligate carriers and controls, indicating that this measurement could not be used for heterozygote detection. In each of the three groups bromide reabsorption was greater than chloride reabsorption. This finding is consistent with a size-dependent anion channel in the sweat epithelial cell because bromide has a smaller hydrated radius than chloride.

Absorption↗

PubMed1984

Collateral reinnervation of sweat glands.

The collateral reinnervation of mouse sweat glands has been studied by a method that allows serial evaluation of the course of reinnervation in intact animals. The method is based on the finding that the activation of secretion from newly denervated sweat glands by pilocarpine or nerve stimulation is completely absent seven days after nerve section but returns with reinnervation. These characteristics allowed serial detection of footpad sweat glands newly reinnervated by collateral sprouting of the remaining intact saphenous nerve after section of the sciatic nerve. The number of saphenous innervated glands increased five- to sevenfold and the total saphenous sweat territory was greatly expanded across the volar surface of the hind paw. There was less enlargement when the sciatic nerve was allowed to regenerate and participate in reinnervation of sweat glands. None of the reinnervated glands were dually innervated by saphenous and sciatic nerves, as is the case in normal glands. When the saphenous nerve was sectioned after saphenous collateral sprouting was complete and after sciatic regeneration had innervated an apparent maximal number of glands, the sciatic nerve reacted by advancing farther into the formerly enlarged saphenous territory and re-reinnervated many of the glands. Collateral sprouting by sudomotor axons is more abundant and more widely dispersed than reported for larger nerve fibers to skeletal muscle and to low-threshold mechanoreceptors. It more closely resembles sprouting of nociceptive axons.

Animals↗

PubMed1994

Quantitative sweat testing using acetylcholine for direct and axon reflex mediated stimulation with silicone mold recording; controls versus neuropathic diabetics.

Sweat glands were stimulated by iontophoresed acetylcholine (ACh). Using a two-chamber capsule, one group of sweat glands was stimulated directly by ACh, and another stimulated indirectly via axon reflexes. Sweat droplets were recorded with a silicone mold and counted by a dissecting microscope and a computerized scanner. Responses from 32 diabetics with generalized somatic peripheral neuropathy were compared with 32 controls. Counting sweat droplets by computerized scanning was more accurate than by microscope. The numbers of droplets, their total areas, and mean areas were all larger in the direct response. Counts of droplet numbers was more diagnostically useful than measuring the total area and the mean areas of the droplets. There was a high correlation between droplet numbers of the direct and the indirect sweat responses. Droplet number counts of the direct response had a slightly higher diagnostic yield than those of the technically more complicated indirect response: for a specificity of 95%, the direct response had a sensitivity of 55%, the indirect being 50%.

Acetylcholine↗

PubMed1991

Baseline water loss and cholinergic sweat stimulation in atopic dermatitis: a gravimetric measurement of local skin water loss.

The sweat gland function in atopic dermatitis (AD) and in respiratory atopy is a matter of controversy. We examined the baseline water loss and local sweating response in non-eczematous back skin of 146 young men: pure AD, AD with rhinitis/asthma, rhinitis/asthma alone, non-atopic dermatosis and non-atopic healthy. All AD subjects were further divided into the subgroups AD dry and AD normal skin. Following injections of saline and a high concentration of methacholine (5 x 10(4) mol/l) into separate sites the moisture losses were collected into closed pads over a period of 40 min. The baseline water loss was significantly increased (P less than 0.001) and median pure sweat loss was significantly decreased (P less than 0.01) in AD compared with nonatopic healthy individuals. These trends were accentuated in AD dry skin. Respiratory symptoms had no appreciable influence on results. A depressed sweating response occurred in 30% of AD subjects and 9% of non-AD subjects. An elevated baseline water loss value and a depressed sweat loss value coexisted in 22% of subjects with AD dry skin compared with 3% of the non-atopics.

Acetylcholine↗

PubMed1991

Individual response to physical work in the heat in relation to sweating and skin blood flow.

The aim of the present study was to examine heart rate and rectal temperature responses to dynamic exercise in a hot environment and their relationship to sweating and skin blood flow. Eight physically trained men were the study subjects. The experiments consisted of 60-min bicycle ergometer tests at intensities of 50 and 100 W in the heat (36 degrees C/30% relative humidity). During the tests, oxygen consumption, heart rate, rectal temperature, and skin temperatures on eight sites were measured. The whole-body sweat rate and evaporation rate and the rate of dripping sweat were measured by a continuous weighing technique. Skin blood flow was estimated from the changes in forearm blood flow. In all, 13 tests were done at 50 W and 10 tests were conducted at 100 W. At 50 W, a physiological steady state was attained in all tests, i.e. the rise in heart rate was less than 10 beats min-1. At 100 W, in all experiments the heart rate and rectal temperature increased continuously throughout the tests. At the end of exercise, the heart rate varied from 98 to 150 beats min-1. At 50 W work load, the heart rate and rectal temperature did not significantly correlate with any of the thermoregulatory parameters. At 100 W, the heart rate and rectal temperature correlated with the total sweat rate (r = -0.66 and -0.71, respectively; P less than 0.05), with the onset of dripping (r = 0.74 and 0.66, respectively, P less than 0.05), and with the ratio of forearm blood flow to dripping sweat rate (r = 0.83 and 0.85, respectively; P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Sweating patterns in atopic dermatitis patients.

Postganglionic sweat output in ten patients with atopic dermatitis was determined by a quantitative sudomotor axon reflex test in which the output results from axon reflex stimulation by acetylcholine iontophoresis. All measurements were obtained from normal skin on the volar aspect of the left wrist and dorsal aspect of the left foot of the atopic patients. Latency, sweat volume, and dynamic sweat pattern were variables included in the study. An abnormal value or configuration was found in nine of the ten patients studied. Seven of the ten patients had abnormal sweat output values. Atopic patients have abnormal sweating patterns, which may be inherently responsible for or related to their disorder.

Acetylcholine↗

PubMed1978

Ultramicro-electrophoresis of protein in sweat from patients with cystic fibrosis of the pancreas and controls.

UNLABELLED: 46 sweat-samples from 32 children with cystic fibrosis of the pancreas (C.F.) and 35 samples from 23 control-children were collected with glass micro-capillaries. Protein was determined by ultramicro-electrophoresis. RESULTS: 1. Protein was detected in 48% of the samples (C.F. and controls). 2. At pH 2.3, C.F.-sweat showed at least one more band than control-sweat. 3. At pH 8.9, C.F.-sweat occasionally showed one more band than the control-group. 4. At pH 2.3, more protein was found at the electrophoresis start point using C.F.-sweat, whereas at pH 8.9 the opposite was found. 5. At pH 2.3, protein was found in fewer samples than at pH 8.9. The "C.F.-factor" is postulated to represent a basic polyelectrolyte which induces the following pathogenic mechanisms: a) Aggregation of proteins giving rise to a high viscosity of secretions, such as saliva. b) Binding to the cell-membrane of the glandular epithelium, thus inducing a disturbance of active NaCl-reabsorption (e.g. by reduction of luminal passive Na+-influx).

Adolescent↗

PubMed1995

Effect of a low-carbohydrate diet on plasma and sweat ammonia concentrations during prolonged nonexhausting exercise.

The purpose of this investigation was to examine the effect of low body glycogen stores on plasma ammonia concentration and sweat ammonia excretion during prolonged, nonexhausting exercise of moderate intensity. On two occasions seven healthy untrained men pedalled on a cycle ergometer for 60 min at 50% of their predetermined maximal O2 uptakes (VO2max) firstly, following 3 days on a normal mixed diet (N-diet) (60% carbohydrates, 25% fat and 15% protein) and secondly, following 3 days on a low-carbohydrate diet (LC-diet) (less than 5% carbohydrates, 50% fat and 45% protein) of equal energy content. Blood was collected from the antecubital vein immediately before, at 30th and at 60th min of exercise. Sweat was collected from the hypogastric region using gauze pads. It was shown that plasma ammonia concentrations after the LC-diet were higher than after the N-diet at both the 30th and 60th min of exercise. Sweat ammonia concentration and total ammonia loss through the sweat were also higher after the LC-diet. The higher ammonia concentrations in plasma and sweat after the LC-diet would seem to indicate an increased ammonia production, which may be related to reduced initial carbohydrate stores.

Adult↗

PubMed1991

Leg skin temperature and thigh sweat output: possible central influence of local thermal inputs.

To demonstrate whether or not the skin temperature of one lower limb can have an influence on the sweat rate of the contralateral leg, the two legs of five subjects were exposed inside leg-chambers to specific local thermal conditions while sweat rates were measured on both limbs. Three experiments (C I, II, III) of 3 h were carried out: each included two phases A and B. During A, the right leg was not ventilated, while the left leg was (C I) or was not (C II-III) ventilated. During B, the legs were either removed from the leg-chambers (C I) or ventilated inside the chambers at differently controlled levels of leg skin temperature (C II-III). At all times, sweat capsules on both legs measured the sweat rates of local areas of the thigh which were also temperature-controlled. Results showed that, at constant or slightly increased mean skin and core temperatures, the sweat output of one leg could be decreased at constant (C II) or higher local skin temperature (C III) probably due to a decrease in the temperature of the opposite leg. This finding is interpreted as a consequence of a central negative effect, originating from contralateral thermal inputs.

Adult↗

PubMed1993

Regulation of local sweating in sleep-deprived exercising humans.

Thermoregulatory sweating [total body (msw,b), chest (msw,c) and thigh (msw,t) sweating], body temperatures [oesophageal (T(oes)) and mean skin temperature (Tsk)] and heart rate were investigated in five sleep-deprived subjects (kept awake for 27 h) while exercising on a cycle (45 min at approximately 50% maximal oxygen consumption) in moderate heat (T(air) and T(wall) at 35 degrees C). The msw,c and msw,t were measured under local thermal clamp (Tsk,l), set at 35.5 degrees C. After sleep deprivation, neither the levels of body temperatures (T(oes), Tsk) nor the levels of msw,b, msw,c or msw,t differed from control at rest or during exercise steady state. During the transient phase of exercise (when Tsk and Tsk,l were unvarying), the msw,c and msw,t changes were positively correlated with those of T(oes). The slopes of the msw,c versus T(oes) or msw,t versus T(oes) relationships remained unchanged between control and sleep-loss experiments. Thus the slopes of the local sweating versus T(oes) relationships (msw,c and msw,t sweating data pooled which reached 1.05 (SEM 0.14) mg.cm-2.min-1.degree C-1 and 1.14 (SEM 0.18) mg.cm-2.min-1.degree C-1 before and after sleep deprivation) respectively did not differ. However, in our experiment, sleep deprivation significantly increased the T(oes) threshold for the onset of both msw,c and msw,t (+0.3 degrees C, P < 0.001). From our investigations it would seem that the delayed core temperature for sweating onset in sleep-deprived humans, while exercising moderately in the heat, is likely to have been due to alterations occurring at the central level.

Adult↗

PubMed1997

Sweat urea, uric acid and creatinine concentrations in uraemic patients.

Concentrations of creatinine, uric acid and urea were measured in the blood and urine of female patients at the final stage of renal disease and on a regular lifelong programme of haemodialysis. The samples were collected in winter-time and in summertime. The same analytes were also measured in sweat fluid at the time of collecting summer samples. The results showed insignificant physiological seasonal changes for creatinine and uric acid and that the concentration of these compounds in the sweat fluid was low. Urea concentration in the sweat fluid was found to be present at a much higher concentration than the serum level (reaching in some cases 50 times the serum level). The possibility of using thermal induction as an alternative to haemodialysis is suggested. The presence of urea in the sweat fluid at such a high level suggests a selective transport mechanism across the eccrine sweat gland to clear the blood of a high urea level.

Adult↗