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PubMed1997

Exercise-induced sweat nitrogen excretion: evaluation of a regional collection method using gauze pads.

The exercise-induced sweat nitrogen excretion was investigated during a 45-minute run at moderate intensity on a treadmill. Sweat was collected with a regional collection technique using gauze pads and compared with the whole-body wash-down (WBW) method. In the regional collection, sweat was sampled from the upper back (UB), lower back (LB), abdomen (AB), and thigh (TH). Additionally, the relation of sweat urea, ammonia, and amino acids was investigated with the regional collection method during a second 45-minute run. Independent of the sweat collection method, a significant and positive correlation was found between sweat rate and the excretion rate of the largest nitrogen fraction urea, suggesting that the sweating response to exercise might be one of the most important factors determining absolute sweat nitrogen losses. The urea nitrogen excretion was nearly 140 mg.h-1 in the second run, representing the largest nitrogen fraction. Ammonia nitrogen and amino acid-derived nitrogen rate were approximately 30 mg.h-1 and 10 mg.h-1, respectively. The comparison of the sampling methods during the first run revealed that the urea nitrogen rate was significantly higher, but the ammonia nitrogen rate significantly lower in the WBW. After summing urea and ammonia nitrogen, no significant difference between the methods was observed anymore, except for UB. It is concluded that the regional collection method using gauze pads is a valuable approach to measure exercise-induced sweat nitrogen losses during moderate running exercise.

Adult↗

PubMed1997

A randomised controlled trial of topical glycopyrrolate, the first specific treatment for diabetic gustatory sweating.

The treatment of gustatory sweating in diabetes mellitus is usually with oral anti-cholinergic drugs, but these frequently lead to unacceptable side effects. Glycopyrrolate is an anti-muscarinic agent that can be applied topically and is efficacious in gustatory sweating occurring in other conditions. In a double-blind placebo-controlled crossover study, we assessed the value of glycopyrrolate in 13 diabetic patients with gustatory sweating. Sweating was measured by a sweat challenge, and diaries recorded by the patients throughout the 2 weeks of each treatment period. Compared to placebo, glycopyrrolate reduced the sweat response to a challenge by 82% (p < 0.01). The frequency of episodes of gustatory sweating during the treatment period was also reduced by 51% (p < 0.01), with a nearly 100% reduction in the frequency of episodes of severe sweating (p < 0.01). In conclusion, topically applied glycopyrrolate is a very effective treatment in reducing both the severity and frequency of diabetic gustatory sweating.

Administration, Topical↗

PubMed1979

Effects of baroreceptor activation on spontaneous activity in the sweat glands and nictitating membrane of the cat.

(1) In chloralose-anesthetized cats, elevation of carotid sinus pressure caused blood pressure, sweat gland potentials and nictitating membrane tension to decrease. (2) The onset and recovery of the sweat gland and nictitating membrane responses usually preceded the respective phases of the blood pressure (depressor) response; the latencies of the sweat gland and nictitating membrane responses agreed with the latencies predicted for neural reflex pathways. (3) The sweat gland and nictitating membrane responses were evoked less consistently than the depressor response. (4) In experiments where only the sweat gland potentials and blood pressure were studied: (a) the sinus pressure threshold for inhibition of sweat gland activity was similar to the threshold for the depressor response; (b) cutting the sinus nerves, or blocking the efferent neural activity to the sweat glands, eliminated the effects of sinus pressure elevation on the sweat gland potentials; (c) with carotid sinus pressure held constant, decreases in blood pressure, produced by stimulating the peripheral end of the vagus nerve, did not affect the sweat gland potentials. (5) These results indicate that baroreceptors can reflexly modulate activity in sympathetic neurons whose target organs are not fundamentally involved in blood pressure regulation.

Adrenergic Fibers↗

PubMed1985

Copper and iron complexes catalytic for oxygen radical reactions in sweat from human athletes.

Sweat collected from 'explosive' and 'endurance' athletes immediately after exercise contains low molecular mass complexes of copper detectable by their ability to bind to o-phenanthroline. Concentrations of these copper complexes are much greater in arm sweat than in trunk sweat. The iron content of arm sweat, as determined by the ferrozine method, is also greater than that of trunk sweat. However, much of the iron in trunk sweat exists in a low molecular mass form that can bind to the antibiotic bleomycin, whereas the iron in arm sweat does not exist in this form. The metal complexes in human sweat are capable of stimulating the peroxidation of membrane lipids in the presence of ascorbic acid. The physiological significance of the presence of iron and copper complexes in sweat is discussed.

Anemia↗

PubMed1994

Rewarming and sweating during cardiopulmonary bypass.

The hypothesis was tested that facial sweating at the end of cardiopulmonary bypass (CPB) is a thermoregulatory phenomenon. Twenty-two patients undergoing cardiac surgery with fentanyl anesthesia were studied. Nasopharyngeal temperature, nasal skin temperature, rectal temperature, and mean skin temperature were monitored for 90 minutes after the start of rewarming on CPB. Calf-toe and forehead-nose skin temperature gradients were followed as a measure of peripheral and facial thermoregulatory vasoactive responses. Facial sweating was defined as grade 1 (noticeable) or grade 2 (obvious droplets). Fourteen patients (64%) sweated during rewarming at the end of CPB. In 11 cases the onset of sweating was preceded by a dramatic increase in nasal skin temperature (mean +/- SEM, 4.6 +/- 0.3 degrees C in 5 min), suggesting facial vasodilation. The maximum rate of increase (degree C/5 min) in nasal skin temperature was significantly greater in patients who sweated than in those who did not, 4.1 +/- 0.4 degrees C versus 2.6 +/- 0.3 degrees C (P < 0.015). There was no difference in the age, weight, or BSA between patients who sweated during CPB and those who did not. The nasopharyngeal temperature threshold for the onset of sweating was not elevated (grade 1, 36.4 +/- 0.5 degrees C; grade 2, 37.6 +/- 0.4 degrees C), but there was a 5 to 6 degrees C interpatient variation. It was concluded that facial sweating during rewarming on CPB is typical of a thermoregulatory response. Absence of sweating in one third of patients may be due to pharmacokinetic or pharmacodynamic differences in the response to anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2005

Responsiveness to autologous sweat and serum in cholinergic urticaria classifies its clinical subtypes.

BACKGROUND: It has been reported that patients with cholinergic urticaria have a type 1 allergy to autologous sweat; however, the pathogenesis of that disorder has not been fully elucidated. OBJECTIVE: We investigated the responsiveness to autologous sweat and serum in patients with cholinergic urticaria in relation to their clinical characteristics. We further classified the clinical subtypes that are clearly characterized by responsiveness to in vivo and in vitro tests as well as their clinical features. METHODS: Intradermal tests with autologous sweat and serum were performed in 18 patients with cholinergic urticaria. Histamine release from peripheral blood basophils induced by autologous sweat was measured. RESULTS: Eleven of 17 patients with cholinergic urticaria showed positive reactions in skin tests with their own diluted sweat. Substantial amounts of sweat-induced histamine release from autologous basophils were observed in 10 of 17 patients. Eight of 15 patients with cholinergic urticaria showed positive reactions in the autologous serum skin tests. All 6 patients who developed satellite wheals after the acetylcholine test showed hypersensitivity to sweat. Further, patients whose eruptions were coincident with hair follicles showed positive responses to the skin test with autologous serum, whereas patients whose eruptions were not coincident with hair follicles did not. CONCLUSION: On the basis of these findings, we propose that cholinergic urticaria should be classified into 2 distinct subtypes. The first (nonfollicular) subtype shows strong positive reactions to autologous sweat and negative reactions to autologous serum. The second (follicular) subtype shows weak reactions to autologous sweat and positive reactions to autologous serum.

Acetylcholine↗

PubMed2002

Structure and function of human sweat glands studied with histochemistry and cytochemistry.

The basic structure and the physiological function of human sweat glands were reviewed. Histochemical and cytochemical techniques greatly contributed the elucidation of the ionic mechanism of sweat secretion. X-ray microanalysis using freeze-dried cryosections clarified the level of Na, K, and Cl in each secretory cell of the human sweat gland. Enzyme cytochemistry, immunohistochemistry and autoradiography elucidated the localization of Na,K-ATPase. These data supported the idea that human eccrine sweat is produced by the model of N-K-2Cl cotransport. Cationic colloidal gold localizes anionic sites on histological sections. Human eccrine and apocrine sweat glands showed completely different localization and enzyme sensitivity of anionic sites studied with cationic gold. Human sweat glands have many immunohistochemical markers. Some of them are specific to apocrine sweat glands, although many of them stain both eccrine and apocrine sweat glands. Histochemical techniques, especially immunohistochemistry using a confocal laser scanning microscope and in situ hybridization, will further clarify the relationship of the structure and function in human sweat glands.

Apocrine Glands↗

PubMed2003

Measuring outcome in cocaine clinical trials: a comparison of sweat patches with urine toxicology and participant self-report.

AIMS: To evaluate the advantages of using a sweat patch (PharmCheck) for detecting cocaine abuse in cocaine-dependent patients participating in a clinical trial. The utility of the sweat patch was assessed from the following perspectives: the reliability and validity of quantitative sweat patch results, the possible degradation of cocaine to benzoylecgonine (BE) as a function of the length of time that a patch is worn, the completeness of the dataset yielded by thrice-weekly urine toxicology compared with thrice-weekly and weekly sweat patches, and the relative costs associated with sweat patch versus urine measures. DESIGN: Data were collected during a 10-week out-patient clinical trial in which participants wore two sweat patches, one applied every visit and one applied weekly. Urine samples were collected thrice weekly, as were self-reports of substance use. SETTING: A multi-site clinical trial conducted in Boston, Cincinnati and New York, USA. PARTICIPANTS: Twenty-seven participants with comorbid diagnoses of cocaine dependence and adult attention deficit disorder completed the study. MEASUREMENTS: Sweat patch and urine samples were analyzed by standard methods for cocaine and cocaine metabolites. FINDINGS: Quantitative sweat patch measures had good reliability in that the correlation between the weekly and per-visit patches was 0.96 (P < 0.0001). The concurrent validity, as judged by the correlation between quantitative urine BE levels and either weekly (0.76, P < 0.0001) or per-visit (0.73, P < 0.0001) cocaine sweat patch levels was reasonable. The correlation between the self-report of cocaine use and these same two patches, however, was lower (0.40, P < 0.05 and 0.30, P < 0.05, respectively). The results revealed no significant degradation of cocaine to BE associated with wearing the patch for a longer time. Finally, the per-visit patch provided cocaine use data on 80.5% of all study days (a total of 70), while urine toxicology and the weekly patch provided 77.4% and 76.1%, respectively. CONCLUSIONS: The present findings suggest that the PharmCheck patch might be an attractive alternative to urine toxicology for use as an outcome measure in cocaine clinical trials.

Adult↗

PubMed2002

Functional requirement of aquaporin-5 in plasma membranes of sweat glands.

The distribution and function of aquaporins (AQPs) have not previously been defined in sweat glands. In this study, AQP1, AQP3, and AQP5 mRNA were demonstrated in rat paw by reverse transcription (RT)-PCR, but AQP2 and AQP4 were not. AQP1, AQP3, and AQP5 protein were confirmed in these tissues by immunoblotting. AQP1 was identified in capillary endothelial cells by immunohistochemical labeling, but not in sweat glands or epidermis. Abundant AQP3 expression was seen in basal levels of epidermis, but not in sweat glands. AQP2 and AQP4 were not observed in either skin or sweat glands. Immunohistochemical labeling revealed abundant AQP5 in secretory parts of rat and mouse sweat glands, where immunoelectron microscopy demonstrated abundant AQP5 labeling in the apical plasma membrane. AQP5 immunolabeling of human sweat glands yielded a similar pattern. To establish the role of AQP5 in sweat secretion, we tested the response of adult mice to s.c. injection of pilocarpine, as visualized by reaction of secreted amylase with iodine/starch. The number of active sweat glands was dramatically reduced in AQP5-null (-/-) mice compared with heterozygous (+/-) and wild-type (+/+) mice. We conclude that the presence of AQP5 in plasma membranes of sweat glands is essential for secretion, providing potential insight into mechanisms underlying mammalian thermoregulation, tactile sensitivity, and the pathophysiology of hyperhidrosis.

Animals↗

PubMed1976

The effects of sweat nitrogen losses in evaluating protein utilization by preadolescent children.

A nitrogen balance study was conducted to determine the effects of three levels of nitrogen intake on the loss of nitrogen through sweat and to assess further the impact of sweat nitrogen on protein needs of preadolescent children. Values were determined through the collection of 24-hr, total body sweat samples from twelve healthy boys having a mean age of 8 years, 8 months. Mean height and weight of the subjects were 131.4 cm and 31.0 kg, respectively. Environmental conditions were relatively constant during the study. Mean sweat nitrogen losses were 208, 287, and 368 mg/day on daily protein intakes of 29, 54, and 84 g, respectively. Mean nitrogen balances per day were 0.39, 0.09, and 1.95 g when sweat nitrogen losses were included in the calculations. At the lower and moderate levels of protein intake, nine and six subjects were in negative nitrogen balance when sweat losses were considered. Sweat nitrogen losses in the boys were similar to a previous study with preadolescent girls. Based upon published basal metabolic rates and mean sweat nitrogen losses of 261 and 288 mg/day for girls and boys, the nitrogen lost through sweat was 0.25 mg/basal kcal for both sexes. An estimation of 0.5 mg/basal kcal for integumental nitrogen loss appears realistic for this age group.

Body Surface Area↗

PubMed2006

Semi-purification of the immunoglobulin E-sweat antigen acting on mast cells and basophils in atopic dermatitis.

BACKGROUND: Sweating aggravates the symptoms of atopic dermatitis (AD). We have recently reported positive skin reactions and histamine release from basophils in response to autologous sweat in patients with AD. OBJECTIVE: To characterize the biochemical and immunological properties of the substance in sweat that evokes histamine release and to study the usability of the basophil-histamine release test with the sweat antigen for AD. METHODS: Sweat collected from healthy volunteers was purified using chromatographies. Serum immunoglobulin (Ig)E of four patients with AD were purified using an affinity-chromatography column with anti-IgE antibodies. The amount of semi-purified sweat antigen (138 ng protein/ml) that induced a half-maximum reaction of basophils of a patient with AD was utilized for the basophil histamine release test. The involvement of specific IgE and high-affinity IgE receptor (FcepsilonRI) in the reactions was examined using basophils of healthy volunteers, a human mast cell line (LAD2), and a rat basophilic leukemia cell line transfected with human alpha-subunit of FcepsilonRI (RBL-48). RESULTS: The semi-purified sweat antigen induced histamine release from the basophils of 47 of 61 (74.6%) patients with AD and four of 46 (8.7%) healthy controls. Both basophils and mast cells sensitized with the patient-derived IgE showed degranulation upon stimulation with the sweat antigen. However, no reaction was observed when cells were sensitized with myeloma IgE or the antigen was treated with proteases. CONCLUSION: The semi-purified standardized sweat antigen consists of a protein that induces degranulation of basophils and mast cells via antigen-specific IgE and FcepsilonRI in patients with AD.

Adolescent↗

PubMed1993

Urokinase-type plasminogen activator in human eccrine sweat.

The presence of urokinase-type plasminogen activator (uPA) in human eccrine sweat has not been reported previously. Clean sweat was obtained from the upper trunk and arms of subjects which had been painted with white petrolatum to minimize epidermal contamination. Sweat was concentrated x 50 by ultrafiltration, and its PA activity determined by the two-step assay method (conversion of plasminogen to plasmin with the subsequent assay of plasmin activity using the substrate S-2251). PA activity was detectable in nine of 17 subjects by this method, which probably represents an underestimate of the true activity because of possible loss of the enzyme during concentration. Scraped (crude) sweat samples contained less PA activity. Sephacryl S-200 gel chromatography of the PA-positive pooled sweat showed a major peak of PA activity at M(r) 55,000. Gelatin-polyacrylamide enzymography revealed a major PA band at M(r) 55,000 and a minor band at 33,000. Sweat PA activity was 94% inhibited by epidermal PA inhibitor and anti-uPA IgG, but not by anti-tPA IgG. We conclude that the PA activity in sweat is derived from the sweat gland and is most likely of the urokinase type. The physiological significance of sweat uPA remains to be determined.

Adolescent↗

PubMed2006

Sweat testing for cystic fibrosis: A review of New Zealand laboratories.

BACKGROUND: Evolving diagnostic criteria for cystic fibrosis, broadening of the populations being tested and the need to interpret intermediate sweat test results have imposed a much greater need to standardize the collection and analysis of sweat. AIM: To identify variations in sweat testing in New Zealand laboratories and compare these with guidelines from the UK and the USA. METHODS: All laboratories in New Zealand offering sweat testing were identified and data collected from these laboratories by structured questionnaire. RESULTS: There were no New Zealand laboratories that conformed to either set of guidelines. Inconsistencies were observed in minimum sweat quantities, the nature of the iontophoresis solution, the sweat electrolytes analysed, quoted reference ranges and recommendations made as a consequence of the result. CONCLUSIONS: Conformity to the guidelines would help to minimize variation in sweat testing in New Zealand. Performance of a sufficient number of tests to maintain expertise is critical, but geographical constraints make patient travel to distant centres difficult in a small, scattered population. A possible solution, where numbers permit, may be the collection of sweat locally, with referral to a major laboratory for analysis. This is only possible with adequate training in collection and follow-up audit of the sweat testing procedure both in the collection and in the analytical phase.

Chemistry, Clinical↗

PubMed1969

Sweat gland function of the donkey (Equus asinus).

1. Donkeys sweat on exposure to heat and in response to intravenous adrenaline infusion.2. Thermal sweating was abolished by the adrenergic-neurone blocking agent bethanidine but not by atropine.3. Sympathetic decentralization (by preganglionic sympathectomy) abolished thermal sweating but adreno-medullary denervation had no effect.4. Exercise resulted in sweating from both sympathetically innervated and decentralized skin and from the innervated skin of animals which had previously undergone adreno-medullary denervation.5. Insulin-induced hypoglycaemia resulted in sweating from sympathetically decentralized skin and from innervated skin in two out of four animals. Adreno-medullary denervation abolished the sweat gland response to insulin administration.6. Cold exposure inhibited the response of innervated sweat glands but not that of decentralized glands to adrenaline infusion.7. It was concluded that heat-induced and exercise-induced sweating of the donkey is controlled by adrenergic nerves; adreno-medullary secretion may contribute to sweating during exercise, and that cutaneous blood flow is important in the response of the glands to humoral stimulation.

Adrenal Medulla↗

PubMed2002

Sweat iron and zinc losses during prolonged exercise.

The purpose of this study was to examine the effects of a 2-hour exercise bout on sweat iron and zinc concentrations and losses in males and females. Nine male and 9 female recreational cyclists exercised at approximately 50% VO(2peak) in a temperate environment (Ta = 23 degrees C, RH = 51%). Sweat samples were collected for 15 min during each of four 30-min exercise bouts. No significant differences were observed between males' and females' sweat iron or zinc concentrations or losses. Sweat iron concentrations decreased significantly between 60 and 90 min of exercise. Sweating rates increased significantly from 30 to 60 min and remained constant during the second hour. Sweat iron losses were significantly lower during the second hour (0.042 mg/m2/h) than the first hour of exercise (0.060 mg/m2/h). Sweat zinc concentrations also decreased significantly over the 2-hour exercise bout. Dietary intakes of iron and zinc were not significantly correlated to sweat iron and zinc concentrations. Sweat iron and zinc losses during 2 hours of exercise represented 3% and 1% of the RDA for iron and 9% and 8% of the RDA for zinc for men and women, respectively. These results suggest a possible iron conservation that prevents excessive iron loss during prolonged exercise.

Adult↗

PubMed1977

Limitations of diagnostic value of the sweat test.

The sweat test, even if carried out by an experienced technician, sometimes lacks reproducibility owing presumably to physiological variations (patient's diet, temperature, and other factors at present unrecognized). Some patients are particularly prone to exhibit this variability and in them a single sweat test is almost valueless. The aldosterone status is believed to be responsible for a reciprocal relationship between sweat sodium and potassium concentrations: tests done on 8 patients show that a high sweat potassium is associated with a correspondingly lower sodium--a circumstance which must be borne in mind when interpreting a patient's sweat sodium. Of 30 patients presenting with a variety of symptoms compatible with a diagnosis of cystic fibrosis and with sweat sodium ranging from 50 to 75 mEq/1 (50-75 mmol/1), only 4 have proved to have cystic fibrosis after several years of observations; 13 have later been diagnosed as having asthma. The problem of the 'grey area' of uncertainty is aggravated by the heterozygous state which is also associated with a sweat sodium in this range. Repeated sweat tests are indicated if the sweat sodium lies within the 'grey area', and the diagnostic importance accorded the test should diminish as the sodium value approaches this area. The diagnosis of cystic fibrosis must remain in doubt unless there is strong supportive clinical evidence.

Adolescent↗

PubMed1991

Spinal mediation of thermally induced sweating.

The sweat responses of nine patients with physiologically complete lesions of the spinal cord (six cervical and three thoracic) were recorded by two different techniques while the patients were exposed to elevated environmental temperatures. Oral temperatures, heart rate and respiration were monitored throughout the observational periods. Oral temperature invariably rose during exposure to heat and both heart rate and respiration tended to increase. Sweating was detected on all of the test areas by both the iodine-starch-paper technique and the quinizarin technique, but it was of widely varying intensity in different portions of the body. In the patients with cervical lesions sweating was generally profuse on the head and neck and occurred in progressively decreasing intensity down to the level of the umbilicus. It was invariably present, but only in very low intensity, on the lower extremity. Sweating was frequently present as a result of manipulation of the patient during the initial preparations, but this generally declined or stopped before the heat was turned on. With application of heat, sweating was recruited on previously dry areas or increased in intensity on those areas in which it was previously present. After oral temperature had increased moderately, the heat was turned off and the doors of the chamber opened widely so that the heat stimulus was suddenly removed. Despite a continued rise in oral temperature, sweating stopped or decreased dramatically. These results are interpreted to indicate the direct mediation by the isolated spinal cord of reflex sweating responses to a heat stimulus applied to the skin. The general distribution of sweating was similar to that associated with distension of the urinary bladder, and careful attention was taken to avoid this complication. The distribution of sweating on the patients with lesions in the thoracic cord was quite different, being most obvious and profuse on the lower extremities and lower trunk and completely absent from the upper trunk, head and upper extremities.

Adolescent↗

PubMed1993

Comparison of core threshold temperatures for forehead sweating based on esophageal and rectal temperatures.

A protocol incorporating successive hot and cold water immersions, causing respective warming and cooling of the body, has been used to determine the core threshold for sweating. Disparate results have been reported for the core threshold of sweating, and these have been attributed to the possible existence of core temperature gradients during such a protocol. Spatial and temporal core temperature (Tc, degree C) gradients during dynamic changes in body temperature may give rise to different values of core temperature thresholds for sweating, depending on the Tc measurement site. In addition, during such an immersion protocol skin temperature transients may influence expression of thresholds using esophageal temperature (Tes). With these considerations, the effects of Tc gradients and skin temperature on Tc thresholds for sweating were examined. Subjects (n = 22) were immersed to the neck in 40 degrees C water until Tes reached 38.5 degrees C (phase 1), followed immediately by cooling in 30.6 degrees C water until extinction of sweating was observed (phase 2). Cooling was continued in the latter bath after the sweating extinction until total immersed time reached 50 min or until shivering was initiated (phase 3). During the trials continuous assessment was made of rectal temperature (Tre) and Tes, mean unweighted skin temperature (Tsk, degree C), forehead sweating rate (Esw, g.m-2.min-1), oxygen consumption (VO2, L.min-1), and surface heat flux (Q, W.m-2). With the current protocol it appeared inappropriate to determine the Tc thresholds for onset of sweating, as sweating was initiated prior to any significant displacement of Tc, but was most likely influenced by Tsk and its rate of change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗