SEARCH · PubMed Health

Results for “Sweating”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources

PubMed1993

A modified, local sweat collector for warm and humid conditions.

The purpose of this study was to modify a previously described local sweat collector to facilitate the investigation of sweat rate and composition in a warm (30 degrees C) and humid (relative humidity 80%) environment. The adherence of the collector to the skin was improved and a pouch was appended at the lower end of the collector. The limitations of the closed collector were examined by comparing the local sweat rate and the quantity of electrolyte excreted in sweat with those obtained using a second collector with a wide opening (to permit free evaporation) and by changes in the body mass. Eight subjects performed exercise on a cycle ergometer consisting of four equal periods of 15 min each, at 60% maximal oxygen consumption, with a rest of 5 min between each period. The sweat produced on a local skin area (85 cm2, upper posterior thorax region) was collected at the end of each period, before measuring the body mass on a sensitive (+/- 1 g) platform balance. The mean local sweat rate [2.61 (SEM 0.19) mg.cm-2.min-1] was 2.4 times greater than the pro-rated whole body mass loss but the two were strongly correlated (r = 0.82, P < 0.01). Compared to the open collector, the greater quantity of electrolyte excreted into the closed collector would suggest that the conditions which prevailed in the closed collector, such as a higher local skin temperature, may have affected the function of the sweat gland.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Developmental interactions between sweat glands and the sympathetic neurons which innervate them: effects of delayed innervation on neurotransmitter plasticity and gland maturation.

The neurotransmitter properties of the sympathetic innervation of sweat glands in rat footpads have previously been shown to undergo a striking change during development. When axons first reach the developing glands, they contain catecholamine histofluorescence and immunoreactivity for catecholamine synthetic enzymes. As the glands and their innervation mature, catecholamines disappear and cholinergic and peptidergic properties appear. Final maturation of the sweat glands, assayed by secretory competence, is correlated temporally with the development of cholinergic function in the innervation. To determine if the neurotransmitter phenotype of sympathetic neurons developing in vivo is plastic, if sympathetic targets can play a role in determining neurotransmitter properties of the neurons which innervate them, and if gland maturation is dependent upon its innervation, the normal developmental interaction between sweat glands and their innervation was disrupted. This was accomplished by a single injection of 6-hydroxy-dopamine (6-OHDA) on Postnatal Day 2. Following this treatment, the arrival of noradrenergic sympathetic axons at the developing glands was delayed 7 to 10 days. Like the gland innervation of normal rats, the axons which innervated the sweat glands of 6-OHDA-treated animals acquired cholinergic function and their expression of endogenous catecholamines declined. The change in neurotransmitter properties, however, occurred later in development than in untreated animals and was not always complete. Even in adult animals, some fibers continued to express endogenous catecholamines and many nerve terminals contained a small proportion of small granular vesicles after permanganate fixation. The gland innervation in the 6-OHDA-treated animals also differed from that of normal rats in that immunoreactivity for VIP was not expressed in the majority of glands. It seems likely that following treatment with 6-OHDA sweat glands were innervated both by neurons that would normally have done so and by neurons that would normally have innervated other, noradrenergic targets in the footpads, such as blood vessels. Contact with sweat glands, therefore, appears to suppress noradrenergic function and induce cholinergic function not only in the neurons which normally innervate the glands but also in neurons which ordinarily innervate other targets. Effects of delayed innervation were also observed on target development. The appearance of sensitivity to cholinergic agonists by the sweat glands was coupled with the onset of cholinergic transmission.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗

PubMed2006

Cold-induced sweating syndrome: a report of two cases and demonstration of genetic heterogeneity.

OBJECTIVES: To characterize the specific autonomic disturbances underlying the cold-induced sweating syndrome (CISS), and to describe a novel genetic variant of this rare recessive disorder. The two not previously reported patients had similar dysmorphic features: abnormal facial appearance, high arched palate, low set rotated ears, flexion deformities of elbows and fingers and scoliosis. Most noticeable were their paradoxical sweat responses: cold ambient temperature induced a profuse sweating over the face, arms and trunk but not over the lower limbs; while in the heat very little sweating occurred primarily on the legs. Testing of autonomic functions demonstrated normal cardiovascular reflexes and postganglionic sympathetic efferent functions. Sural nerve morphology and number of unmyelinated fibers was normal and skin biopsies showed normal appearing eccrine sweat glands. MRI scans revealed no structural brain abnormalities. Oral clonidine, prescribed in one patient, completely suppressed cold-induced sweating. Observed clinical features matched those of two sisters reported from Israel and of two brothers reported from Norway. All six cases presented a similar phenotype. The Norwegian, Israeli and Canadian cases were homozygous or compound heterozygous, respectively, for mutations in the CRLF1 gene on chromosome 19p12 (CISS1). The Australian case, however, had no pathogenic sequence variants in the CRLF1 gene, but was compound heterozygous for mutations in the CLCF1 gene on chromosome 11q13.3 (CISS2). CONCLUSION: The rare cold-induced sweating syndrome is genetically heterogeneous and is probably caused by central and peripheral impairment of sudomotor functions. This is the first detailed report on the clinical consequences of mutations in the CLCF1 gene in humans. Directions for medical therapies are outlined to achieve long term symptom control.

Adult↗

PubMed2001

Immunohistochemical study of angiotensin receptors in normal human sweat glands and eccrine poroma.

BACKGROUND: Angiotensin II exerts its actions through its specific receptors. However, expression of these receptors has not been determined in sweat glands. OBJECTIVES: To clarify the expression and localization of the angiotensin receptors in normal human sweat glands and eccrine poroma. METHODS: Expression of angiotensin type 1 (AT1) and type 2 (AT2) receptors in normal human eccrine and apocrine sweat glands and 12 cases of eccrine poroma was studied using immunohistochemistry. RESULTS: In eccrine sweat glands, the acrosyringium and the inner surfaces and luminal cells of the intradermal duct showed positive staining with AT1. In apocrine sweat glands, the intraepithelial duct and luminal cells of the intradermal duct showed positive staining with AT1. In 12 cases of eccrine poroma, some of the tumour cells in the tumour strands and cells surrounding the luminal structures stained positively. There were no positive findings with AT2. CONCLUSIONS: Studying AT1 distribution may be useful in understanding the pathophysiology of sweat glands and sweat gland tumours.

Acrospiroma↗

PubMed1983

Higher bioelectric potentials due to decreased chloride absorption in the sweat glands of patients with cystic fibrosis.

Patients with cystic fibrosis have characteristic disturbances in the electrolyte composition of their sweat, saliva, and pancreatic secretions. We studied the electrical properties of sweat glands in eight patients with cystic fibrosis and in seven normal volunteers to determine the basis of the well-documented inhibition of sodium absorption in this disease. The average electrical potential across 47 sweat glands in the patients was -66.3 +/- 2.1 mV, as compared with -29.8 +/- 3.2 mV for 39 glands in the normal controls (P less than 0.001). The average sweat-secretion rate in 33 glands from six patients was not significantly different from that in 34 glands from six controls, but average concentrations of sodium, chloride, and potassium were significantly higher in sweat droplets from the patients. Calculated rates of both sodium and chloride reabsorption were lower in sweat glands of patients than of normal controls, but chloride reabsorption was more markedly reduced than sodium reabsorption. We conclude that a decrease in epithelial permeability to chloride may explain the characteristic changes in sweat electrolytes in cystic fibrosis and could be a generalized abnormality in the disease.

Absorption↗

PubMed1984

Predominantly beta-adrenergic control of equine sweating.

Single equine sweat glands were found to secrete for more than 1 h in vitro in response to pharmacologic secretagogues. The adrenergic agonists epinephrine and norepinephrine evoked maximal sweat rates of 2.0 nl X gland-1 X min-1. However, the concentration of norepinephrine (10(-5) M) required to evoke the maximal response was 10 times higher than that for epinephrine. Maximal sweat rates also were stimulated with the beta 2-adrenergic agonist terbutaline. This stimulation was blocked by the beta-adrenergic antagonist propranolol. Moderate sweating responses were also obtained with the alpha-adrenergic agonists phenylephrine and methoxamine, but these responses also were blocked by propranolol. Neither the muscarinic blocker atropine nor the alpha-adrenergic antagonist phentolamine inhibited any of the pharmacologically induced sweat responses. Unlike most other mammalian exocrine glands, cholinergic agonists were ineffective in stimulating sweat secretion. Therefore equine sweat glands apparently are under predominantly beta-adrenergic control.

Animals↗

PubMed1983

Human frontal sweat rate and lactate concentration during heat exposure and exercise.

Output (Qsweat) and lactate concentration ( [L]sweat) in frontal sweat and blood lactate concentration ( [L]blood) were monitored in three male volunteers: one sedentary (S), one fit (F), and one very fit (VF). Measurements were made under three sweating conditions: 1) heat exposure to infrared radiation (IR) at rest for 25 min at 45 degrees C; 2) bicycle exercise at constant relative maximal aerobic power (87 +/- 2% MAP) for 25 min (Cst EX) at 23 degrees C; and 3) bicycle exercise at increasing work loads (from 60-95% MAP) in four or five successive 5-min steps (Incr EX) at 23 degrees C. Comparison of these data showed that under the above three conditions 1) Qsweat of S was lower than that of F and VF; and 2) changes in [L]sweat were different: in IR and Cst EX, [L]blood remained constant, and [L]sweat decreased with heat load duration similarly in the three subjects (the slopes of the two curves were not significantly different); at Incr Ex, [L]blood increased and [L]sweat remained constant in S, F, and VF (21.71 +/- 0.85, 16.75 +/- 0.99, 12.83 +/- 0.45 (SE) mM, respectively). It was suggested that the high [L]blood and increased adrenergic stimulation observed in Incr Ex could act on [L]sweat in relation to the physical fitness level.

Adult↗

PubMed1991

Sweat lactate in exercising children and adolescents of varying physical maturity.

This study attempts to explain some of the individual variability in sweating pattern by comparing prepubescents and pubescents. Sweating rate and muscular anaerobic capacity are higher in adults than in children; thus we hypothesized that sweat gland anaerobic metabolism, as reflected by lactate excretion, might be higher with advanced physical maturity (PM). Lactate concentration in sweat ([LAC]sw) was measured at various stages of PM in boys who exercised in the heat. The subjects were divided into three groups on the basis of Tanner staging: prepubertal (PP, n = 16), midpubertal (MP, n = 15), and late pubertal (LP, n = 5). Subjects cycled at 50% of maximal O2 uptake for three 20-min bouts, with 10-min rest periods, in 42 degrees C and 18% relative humidity. Sweat samples were harvested, and population density of activated sweat glands was determined after each exercise bout. [LAC]sw during bout 1 was higher in PP than in LP [PP = 22.2 +/- 2.2, MP = 19.5 +/- 1.4, LP = 14.3 +/- 1.3 (SE) mmol/l]. In all groups, [LAC]sw decreased during subsequent bouts, and there were no intergroup differences in [LAC]sw during bout 3 (PP = 11.2 +/- 0.4, MP = 10.6 +/- 0.5, LP = 9.7 +/- 0.2 mmol/l). [LAC]sw was inversely related to sweating rate. Lactate excretion rate per gland was greater with the increase in PM (PP = 61.0 +/- 8.2, MP = 79.1 +/- 11.3, LP = 99.9 +/- 11.0 pmol/min; P = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2001

Function of human eccrine sweat glands during dynamic exercise and passive heat stress.

The purpose of this study was to identify the pattern of change in the density of activated sweat glands (ASG) and sweat output per gland (SGO) during dynamic constant-workload exercise and passive heat stress. Eight male subjects (22.8 +/- 0.9 yr) exercised at a constant workload (117.5 +/- 4.8 W) and were also passively heated by lower-leg immersion into hot water of 42 degrees C under an ambient temperature of 25 degrees C and relative humidity of 50%. Esophageal temperature, mean skin temperature, sweating rate (SR), and heart rate were measured continuously during both trials. The number of ASG was determined every 4 min after the onset of sweating, whereas SGO was calculated by dividing SR by ASG. During both exercise and passive heating, SR increased abruptly during the first 8 min after onset of sweating, followed by a slower increase. Similarly for both protocols, the number of ASG increased rapidly during the first 8 min after the onset of sweating and then ceased to increase further (P > 0.05). Conversely, SGO increased linearly throughout both perturbations. Our results suggest that changes in forearm sweating rate rely on both ASG and SGO during the initial period of exercise and passive heating, whereas further increases in SR are dependent on increases in SGO.

Acclimatization↗

PubMed1969

Micropuncture studies of the sweat formation in cystic fibrosis patients.

In order to determine whether the precursor solution of sweat is abnormal in cystic fibrosis, osmolality and concentrations of sodium and chloride were measured in fluid obtained by micropuncture from the sweat gland coil of the nail fold of patients with this disease. Osmolality was 323+/-4.8 SE (mOsm/kg of water), sodium concentration was 151+/-1.1 SE (mEq/liter), and chloride concentration was 124+/-6.0 SE (mEq/liter). The sweat:plasma ratio for osmolality averaged 1.1+/-0.015 SE. These values are not significantly different from the corresponding ones obtained previously in normal individuals. It is concluded therefore that the disturbance of sweat gland function as far as electrolytes are concerned is restricted to the excretory ducts. In a second series of experiments the stop-flow pressure which is generated by sweat glands during secretion was measured. Values up to 500 mm Hg were found in both patients and normals. According to van't Hoff's law (DeltaP = RTDeltaC) hydrostatic pressure differences of this magnitude can be generated by the osmotic difference of 27 mOsm/kg of water observed between precursor sweat and plasma in the present experiments. With respect to the mechanism of sweat secretion this finding supports the hypothesis that active solute transport creates an osmotic gradient which causes osmotic water flux.

Adolescent↗

PubMed1977

Problems associated with measuring sweat chloride concentration with an ion-specific electrode.

The measurement of sweat chloride concentration was investigated by using the Orion 417 skin chloride electrode. The effects of variation in pilocarpine concentration, iontophoresis period, and sweat collection period were also investigated. The results show that the sweat chloride concentration is directly related to the amount of sweat produced. When the amount of sweat collected falls below a certain level, there is an apparent increase in sweat chloride concentration. A procedure is recommended for the measurement of sweat chloride concentration which offers good precision (coefficient of variation 9.8%) and the minimum of inconvenience to the patient.

Adult↗

PubMed1984

The sweating deficiency in diabetes mellitus: methods of quantitation and clinical correlation.

A method that measures the amount of sweat evaporating from the skin was used to quantitate the sweating deficiency that accompanies diabetic neuropathy. The decreased amount of sweat secreted after pilocarpine stimulation was proportional to the reduction in number of excitable sweat glands, and to the decrease in water measured by the summed volume of all sweat droplets secreted. The results also correlated favorably with the degree of sensory loss to painful stimuli, but not to the alpha motor nerve conduction velocity or motor axon loss evaluated by muscle action potentials evoked from foot muscles. Respiratory-cardiovascular reflexes, as measured by the Valsalva ratio, were always abnormal in patients with demonstrated sweating deficiency and often in patients with normal sweat function.

Adult↗

PubMed1987

Local effect of vasoactive intestinal polypeptide on human sweat-gland function.

Physiological significance of vasoactive intestinal polypeptide (VIP), a putative co-transmitter of the cholinergic neuron innervating sweat glands, was investigated by its local effect on drug-induced sweating. VIP, methacholine chloride (MCH), or VIP plus MCH dissolved in 0.1 ml of 0.9% NaCl solution to a specified concentration was injected intradermally at the center of a forearm test area of 15 cm2 and the sweat rate was recorded continuously by capacitance hygrometry. In a cool environment (Ta, 23 degrees C), VIP failed to cause sweat secretion, but increased the rate of MCH-induced sweating, most markedly at a concentration of 10(-5) g/ml, where the rise in local skin temperature was the greatest. On an area anesthetized by nerve block in a hot environment (Ta, 35 degrees C), the effect was less obvious and less consistent, indicating that the sweat-facilitatory effect of VIP is reduced under the condition of passive cutaneous vasodilation. It may be postulated that VIP plays a role in securing ample oxygen supply to functioning sweat glands, especially with a relatively high cutaneous vasoconstrictor tone.

Adult↗

PubMed2000

Noninvasive approach for study of human reaction and transferring velocity of nervous system by using a new instrumentation devised for concurrent microscopic observation and analysis of sweat secretion on human body under 1G and microgravity.

Human sweating is generally caused by thermal and mental stimuli. The former role is well known as a response for thermo regulation. The insensible perspiration may be generally controlled by the autonomic nervous system, and the responses due to mental and/or emotional stress by the sympathetic nervous system. As human sweating is directly concerned with some nervous systems, sweating may be a good indicator for the body reactions of feeling, surprise, emotional stress and etc. The measuring of sweat secretion and microscopic observation of active sweat glands can be presented the direct information of working of sympathetic nervous system and sudomotor. In the present report, we devised an instrumentation for the estimation of time lag of sweating [correction of seating] after physical stimuli. Variation of gravity during parabolic flights is a kind of physical stimulus. Iwase et al reported the changes of sympathetic outflow to muscle in humans during short periods of microgravity. We studied also the variation of number of active sweat glands under this condition for the evaluation of human sympathetic nervous system.

Humans↗

PubMed2006

Thermoregulatory sweat testing in patients with erythromelalgia.

OBJECTIVES: To examine the results of thermoregulatory sweat testing in patients with erythromelalgia and to compare them with the results of other neurophysiologic tests of small-fiber nerve function. DESIGN: Retrospective study. SETTING: Tertiary referral center. PATIENTS: Thirty-two consecutive patients with erythromelalgia who had thermoregulatory sweat testing in addition to vascular and nerve testing. INTERVENTION: The following information was abstracted for each patient: demographics, clinical presentation, and results of thermoregulatory sweat testing, vascular (noninvasive) testing, and nerve testing (electromyography and autonomic reflex screen, including quantitative sudomotor axon reflex test). MAIN OUTCOME MEASURES: Results of thermoregulatory sweat testing to evaluate small-fiber neuropathy, compared with other tools used to estimate small-fiber neuropathy. RESULTS: Thermoregulatory sweat testing results were abnormal in 28 (88%) of 32 patients, and quantitative sudomotor axon reflex test results were abnormal in 22 patients (69%). Abnormalities noted on thermoregulatory sweat testing varied from local hypohidrosis or anhidrosis to global anhidrosis. Global or almost-global anhidrosis was present in 8 patients (25%); in 19 patients (59%) the anhidrosis was distal, and 1 other patient (3%) had a less specific pattern of anhidrosis (multifocal or regional). The area of anhidrosis generally corresponded to the area that was symptomatic of the erythromelalgia. CONCLUSIONS: Small-fiber neuropathy is prevalent in most patients with erythromelalgia. Thermoregulatory sweat testing is a sensitive and useful marker of small-fiber neuropathy in these patients.

Adolescent↗

PubMed1996

Gustatory sweating in diabetes mellitus.

Gustatory sweating has been only rarely reported in diabetes mellitus and is thought to be due to axonal regeneration within the autonomic nervous system. We investigated the relationship of gustatory sweating to other diabetic complications. 196 patients in four groups (diabetic nephropathy, diabetic neuropathy, diabetic controls, and non-diabetic renal failure) were questioned about gustatory sweating. Somatic and autonomic neuropathy were assessed by clinical signs, vibration perception threshold, and heart rate variability. Sixty-nine percent of patients with nephropathy and 36% of those with neuropathy reported gustatory sweating, whereas less than 5% reported it in the other two groups. Five subjects reported that gustatory sweating either disappeared or significantly improved immediately after renal transplantation. Analysis of the nephropathy and neuropathy groups separately showed a strong correlation between gustatory sweating and degree of neuropathy (p < 0.01). This study shows that gustatory sweating is much more common than previously believed and demonstrates that it is often very closely linked with diabetic nephropathy.

Analysis of Variance↗

PubMed2000

Sweat analysis proficiency testing for cystic fibrosis.

The purpose of this report is to describe the College of American Pathologists sweat testing (SW) proficiency testing program for cystic fibrosis, to evaluate its impact on test performance, and to describe the current practice of sweat testing in North America. The study analyzed participant summary reports of the SW survey from 1994-1998 (SW 94-98) and Proficiency Testing Exception Summary reports from 1996-1998. The data collected from SW 94-98 allowed for the assessment of trends and/or changes in sweat testing practices. The data collected from SW-A 1998 provided a profile of current practices in sweat testing. While the overall performance on the SW survey is encouraging, the program has identified areas of concern. The number of poorly performing laboratories are few in number, yet if the reported results had been patient specimens, the clinical implications would have been significant. The SW survey is meeting its goal of providing feedback to institutions on their performance of sweat analysis and providing educational materials on the total testing process in an effort to improve the quality of sweat testing. Significant changes in practice have occurred in many institutions performing sweat tests, and a greater awareness of analyte identification has resulted.

Chlorides↗

PubMed1994

Innervation of footpads of normal and mutant mice lacking sweat glands.

Footpads of normal adult mice are innervated by sympathetic and sensory fibers. The sympathetic fibers associated with sweat glands contain acetylcholinesterase and immunoreactivity for vasoactive intestinal peptide. Although catecholamine histofluorescence is absent, the gland innervation exhibits immunoreactivity for tyrosine hydroxylase. A distinct population of sympathetic fibers, which possess catecholamines and neuropeptide Y as well as tyrosinehydroxylase immunoreactivity, innervates blood vessels. Sensory fibers containing immunoreactivity for substance P and calcitonin gene-related peptide course beneath the epidermis and some form endings in it. Treatment of neonatal mice with the adrenergic neurotoxin, 6-hydroxydopamine, results in loss of sympathetic innervation of sweat glands and blood vessels, permits growth of sensory axons into sweat glands, but does not alter the peptidergic sensory innervation of the dermis and epidermis. Three mouse mutations, Tabby (Ta), crinkled (cr), and downless (dl), disrupt the interactions between the mesenchyme and epidermis that are required for normal development of specific epidermal derivatives, including sweat glands. The sympathetic innervation of blood vessels and sensory innervation of footpad skin of the three mutant mice that lack sweat glands is indistinguishable from normal. The sympathetic fibers that normally innervate sweat glands, however, are not present. These results indicate that in the absence of their normal target, the sympathetic fibers that innervate sweat glands are lacking. Furthermore, they suggest that, although sensory fibers may sprout into sympathetic targets in the footpad, the domains occupied by sensory fibers are not normally accessible to sympathetic axons.

Animals↗