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PubMed1991

Muscarinic M3 receptors mediate secretion from sweat glands in the rat.

We investigated a series of muscarinic antagonists for their ability to inhibit muscarinic-mediated secretions from salivary and sweat glands in the rat. Their potency in blocking saliva secretion was compatible with the inhibition of M3 receptors. A highly significant correlation was found between their potency in blocking secretion from both salivary and sweat glands. These results indicate that salivary and sweat glands possess the same muscarinic receptors which conform to the M3 subtype.

Animals↗

PubMed2000

Absent innervation of skin and sweat glands in congenital insensitivity to pain with anhidrosis.

OBJECTIVES: A case of a 10-year-old girl with congenital insensitivity to pain with anhidrosis (CIPA) is reported. METHODS AND RESULTS: Parents referred several hyperpyretic episodes without sweating occurring since birth, and insensitivity to pain, noticed when the child was 2 years old. Her body had many bruises and scars, bone fractures and signs of self-mutilation. Neurological examination was normal except for insensitivity to pain. Her IQ was 52. Electrical and tactile sensory nerve conduction velocities were normal. The patient was unable to detect thermal stimuli. Histamine injection evoked a wheal but not a flare; pilocarpine by iontophoresis did not induce sweat. Microneurography showed neural activity from A-beta sensory fibers while nociceptive and skin sympathetic C fiber nerve activity was absent. No small myelinated fibers and very rare unmyelinated fibers were found in the sural nerve. Immunohistochemistry showed a lack of nerve fibers in the epidermis and only few hypotrophic and uninnervated sweat glands in the dermis. CONCLUSIONS: The lack of innervation of the skin (C and A-delta fibers) appears to be the morphological basis of insensitivity to pain and anhidrosis, and is consistent with the loss of unmyelinated and small myelinated fibers in the sural nerve biopsy.

Child↗

PubMed2000

Pitfalls in the immunohistochemical localization of the cystic fibrosis transmembrane conductance regulator in paraffin embedded sweat glands.

Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene cause the hereditary disease cystic fibrosis. The most frequent mutant deltaF508 has been shown in vitro to be retained in the endoplasmic reticulum. Ex vivo studies using immunohistochemical labelling in cryofixed skin biopsies have confirmed the mislocalization of deltaF508 CFTR in sweat glands. The purpose of this study was to test CFTR antibodies in paraffin-embedded skin biopsies to take advantage of the superior tissue preservation as compared to cryofixation. A panel of 7 CFTR antibodies was applied to skin sections of healthy controls and of cystic fibrosis patients homozygous for the deltaF508 mutation. Sweat gland labelling consistent with CFTR localization and different between control and cystic fibrosis tissue was obtained with 2 antibodies. Conventional staining controls confirmed the labelling specificity. The antibodies were subsequently tested in a series of 237 sections of 16 biopsy specimens. However, the sweat gland labelling pattern proved not to be dependent on CFTR genotype. This finding was the sole indicator of non-specificity of the staining which was revealed only by the size of our random sample. Our results emphasize that CFTR immunolabelling following formalin fixation has to be interpreted with the utmost caution.

Antibodies, Monoclonal↗

PubMed1983

The metabolism and hormonal responses of human eccrine sweat glands isolated by collagenase digestion.

1. Collagenase digestion of biopsies of human skin yields eccrine sweat glands that can be picked out under binocular light microscopy. The glands are viable as determined by the exclusion of Trypan Blue, the uptake of Methylene Blue, electron microscopy, the rate of lactate dehydrogenase release, ATP content and the rates of glucose oxidation and lactate release. 2. It is proposed that eccrine sweat glands engage in aerobic glycolysis, which accounts for the high content of lactate in sweat (15--60 mM) and the high lactate/pyruvate ratio (100: 1) [Emrich & Zwiebel (1966) Pfluegers Arch. 290, 315--319]. 3. Acetylcholine causes a 4-fold increase in cyclic GMP content, dilatation of the intercellular canaliculi and a reversible, atropine-sensitive, 2-fold increase in the rates of glucose oxidation and lactate release. 4. Isoprenaline causes a 2.5-fold increase in cyclic AMP content. Phenylephrine does not significantly alter cyclic nucleotide metabolism.

Acetylcholine↗

PubMed1985

The human eccrine sweat gland adenylate cyclase system: response to agonists.

Cyclic AMP accumulation has been measured in whole human sweat glands. The mean rate in glands from 19 subjects was 0.519 +/- 0.316 pmol of cyclic AMP formed 5 min-1 micrograms-1 of DNA, which is comparable with that reported for other tissues. Cyclic AMP accumulation in the sweat gland is stimulated fourfold by prostaglandin (PG) E1 and fivefold by PGE2 (0.1 mmol/l), in accord with stimulation in renal tubules and medullary membranes. Bradykinin (10 micrograms/ml) increases the rate threefold and this is substantially prevented by indomethacin (1.5 X 10(-5) mol/l), as also is a fivefold stimulation by cyclic GMP (10(-5) mol/l). Mecholyl (10(-2) mol/l) and isoprenaline (6 X 10(-6) mol/l) increase the rate five- and four-fold respectively, and these agonist effects are largely abolished by atropine and propranolol. The stimulation and inhibition pattern suggests a direct action of PGE, enhancement of prostaglandin synthetase by cyclic GMP and stimulation of guanylate cyclase by mecholyl and bradykinin. Isoprenaline presumably stimulates adenylate cyclase directly. This complex chain of events, from cholinergic stimulation to an enhancement of adenylate cyclase, demonstrated in vitro, constitutes a potential for flexible and fine control of sweat gland function.

Adenylyl Cyclases↗

PubMed2002

CD34-positive stromal cells and alpha-smooth muscle actin-positive stromal cells in the tumor capsule of skin sweat gland neoplasms.

To elucidate the roles of CD34-positive stromal cells and alpha-smooth muscle actin-positive stromal cells at the tumor border of skin sweat gland neoplasms, we examined expression of stromal cell markers in the tumor capsule of 19 skin sweat gland neoplasms (16 mixed tumors of the skin and three nodular hidradenomas) using monoclonal antibodies to CD34, CD31, cytokeratin 14 (CK14), alpha-smooth muscle actin (ASMA) and high molecular weight caldesmon (HCD). We regarded CD34-positive, CD31-, CK14-, ASMA- and HCD-negative stromal cells to be CD34-positive stromal cells, and ASMA-positive, HCD-, CK14-, CD34- and CD31-negative stromal cells to be ASMA-positive stromal cells. CD34-positive stromal cells were detected in the tumor capsule of all 19 of the tumors examined. In nine of the 16 mixed tumors (56%) and all of the three nodular hidradenomas, ASMA-positive stromal cells were detected at the immediate inner side of the CD34-positive stromal cell layers. These results indicate that cellular components in the tumor capsules of mixed tumors of the skin and nodular hidradenomas are CD34-positive stromal cells and ASMA-positive stromal cells, and suggest that stromal cells of these two cell types are associated with tumor capsule formation of skin sweat gland neoplasms.

Actins↗

PubMed2003

Drug-induced sweat gland necrosis in a non-comatose patient: a case presentation.

BACKGROUND: Coma-induced bullae and sweat gland necrosis is a rare clinicopathological entity often associated with drug-induced coma. SUBJECT: We report a case with clinical and histopathologic findings characteristic of blisters and sweat gland necrosis occurring in a non-comatose patient. CONCLUSIONS: Skin blisters with underlying sweat gland necrosis is an entity previously reported to occur in comatose patients, our findings open new questions about the role of the drugs in the pathogenesis of those conditions.

Adult↗

PubMed1998

Re-epithelialization of porcine skin by the sweat apparatus.

The behavior of the keratinocyte during the initial stages of cutaneous wound repair has been the subject of intense investigation. Most of these studies have focused on the lateral edges of wounds as the source of activated keratinocytes. Less attention has been directed towards elucidating the role of the appendageal structures as sources of keratinocytes for re-epithelialization, particularly the sweat apparatus. Surgical wounds of specific depths were created in pig skin, above and below hair follicles, and wound healing was allowed to take place in a setting in which lateral ingrowth of keratinocytes by migration was prevented. In this manner, all re-epithelialization occurred from residual appendageal structures. In those wounds where only sweat gland elements remained, an epithelium formed that had clinical, morphologic, and protein electrophoretic features closer to palmar/plantar or mucosal-like epithelia. In contrast, wounds that retained elements of the hair follicle healed faster and the resultant epithelium clinically, morphologically, and biochemically resembled the surrounding nonwounded epidermis. These findings establish that the sweat apparatus is capable of re-epithelializing the skin surface after a major cutaneous wound, but may not be capable of mimicking the epidermis.

Animals↗

PubMed1975

Inheritance of some sweat gland and hair follicle characteristics in cattle.

Using measurements made in cows in the herds of the Hannah Research Institute (Ayrshire), the West of Scotland Agricultural College (Ayrshire and Friesian) and in the twin herd of the Animal Breeding Research Organisation (Ayrshire), repeatability and heritability estimates were obtained for three hair follicle and four sweat gland traits. Average repeatability was high (50-70%) for all characters except angle of slope of the hair (18%). Heritability estimates were extremely variable among the different herds and methods of measurement but there was evidence of considerable genetic variation, particularly for sweat gland traits. The most consistent heritability estimate (30-45%) was given by the ratio of sweat gland length to diameter. The potential of skin types for the selection of cattle for tropical regions is discussed.

Age Factors↗

PubMed1970

Impedance changes across the footpad of the cat in relation to action and secretion in sweat glands.

Impedance changes across the footpad of the cat occur as the result of sweat gland activity after stimulation of the sudomotor nerves. It is possible to discern two phases of impedance change; one, early, associated with the action potential of sweat gland cells; the other, later, being the well-known change associated with secretion and reabsorption.(1) After a single stimulus, latency for the initial impedance change is about that of the sweat gland cell action potential, that of the secretory change approximately 1 additional second.

Action Potentials↗

PubMed1990

Paradoxical effects of essential fatty acid supplementation on lipid profiles and sweat electrolytes in cystic fibrosis.

Supplements of evening primrose oil (Oenothera biennis), which contains at least 72% linoleic (18:2n-6) and 7% gamma-linolenic (18:3 n-6) acids (expressed as % fatty acid methyl esters) were given to sixteen cystic fibrosis patients for a period of 12 months. Clinical observations showed no significant changes in patients' weights or respiratory function throughout. Linoleic acid levels in plasma and erythrocyte membranes increased significantly during the first 6 months but this increase was not sustained at its initial level. After supplementation was discontinued reversion to baseline (low) levels occurred within 4 months. Levels of plasma prostaglandins (PG) and urinary PG metabolites varied among individuals over a wide range, and urinary PGF2 alpha metabolites fell during the supplementation. There was a significant fall in sweat sodium concentrations after 6 weeks of supplementation, but sweat chloride was unchanged. It is not known whether the effect of essential fatty acids on sweat Na+ reflects changes in cell membrane conformation or if there is a direct effect on Na+ pump activity.

Adolescent↗

PubMed1995

Validation and adjustment of the mathematical prediction model for human sweat rate responses to outdoor environmental conditions.

Under outdoor conditions this model was over estimating sweat loss response in shaded (low solar radiation) environments, and underestimating the response when solar radiation was high (open field areas). The present study was conducted in order to adjust the model to be applicable under outdoor environmental conditions. Four groups of fit acclimated subjects participated in the study. They were exposed to three climatic conditions (30 degrees, 65% rh; 31 degrees C, 40% rh; and 40 degrees C, 20% rh) and three levels of metabolic rate (100, 300 and 450 W) in shaded and sunny areas while wearing shorts, cotton fatigues (BDUs) or protective garments. The original predictive equation for sweat loss was adjusted for the outdoor conditions by evaluating separately the radiative heat exchange, short-wave absorption in the body and long-wave emission from the body to the atmosphere and integrating them in the required evaporation component (Ereq) of the model, as follows: Hr = 1.5SL0.6/I(T) (watt) H1 = 0.047Me.th/I(T) (watt), where SL is solar radiation (W.m-2), Me.th is the Stephan Boltzman constant, and I(T) is the effective clothing insulation coefficient. This adjustment revealed a high correlation between the measured and expected values of sweat loss (r = 0.99, p < 0.0001).

Adolescent↗

PubMed1975

Acclimatization and maximum number of functioning sweat glands in Hindu and Dutch females and males.

The number and distribution of thermally (hot water bath method) activated eccrine sweat glands have been measured in Dutch, Hindu and Bushnegro males and in Dutch and Hindu females in Surinam. Results are compared with those for Dutch and Hindu males and females in the Netherlands. The results suggest that the maximum number of functioning sweat glands (F.S.G.) changes during natural acclimatization and that probably the relative magnitude of this change depends on the percentage of "recruitment type" adapters within each racial group. This change was not apparent for all sixteen body areas studied. In these experiments high relative humidity had no influence on the number of functioning sweat glands. No sex differences were observed in body density or in pattern of regional distribution. Only the Hindu and Dutch males differed significantly in body density. A positive relationship was observed between body density and extremities-weight ratio in the three male groups.

Acclimatization↗

PubMed1979

Zinc retention and losses of zinc in sweat by preadolescent girls.

Preadolescent girls, ages 7 to 9 years, were fed levels of zinc ranging from 5.61 to 14.61 mg/day during an 18-day metabolic study. All other nutrients were provided at or above Recommended Dietary Allowance levels. The sweat loss of zinc was measured using an arm-bag method and whole body zinc loss was calculated from whole body nitrogen and arm loss of nitrogen and zinc. Fecal zinc reflected dietary zinc, but urinary zinc remained relatively stable. The mean daily loss of zinc through sweat was calculated to be 1.43 mg. Zinc retentions were not significantly different (P greater than 0.05) though the retention increased generally with intake of zinc. A comparison of these data with previously reported studies indicated that the absorption of zinc was usually in the range of 20 to 30%. Based on sweat losses reported by others and found in this study and on usual absorption of zinc, it appears that diets should provide a minimum of 7 mg of zinc daily for growing children.

Child↗

PubMed1978

A modified ion-selective electrode method for measurement of chloride in sweat.

A modified method of analysis of sweat chloride concentration with an ion-selective electrode is presented. The original method of sweat chloride analysis proposed by the Orion Research Corporation (Cambridge, Massachusetts 02139) is inadequate because it produces erratic and misleading results. The modified method was compared with the reference quantitative method of Gibson and Cooke. In the modified method, individual electrode pads are cut and placed in the electrodes rather than using the pads supplied by the company; pilocarpine nitrate (2,000 mg/l) is used in place of pilocarpine HCl (640 mg/l); sodium bicarbonate as the weak electrolyte is used instead of K2SO4. A 10-minute period for sweat accumulation is employed rather than a zero-time collection as in the original Orion method. The modification has been studied for reproducibility in individuals, reproducibility between right and left arm in individuals; it has been compared extensively with the quantitative method of Gibson and Cooke, both in normal individuals and in patients with cystic fibrosis. There is excellent agreement between the modified method and the quantitative reference method. There appears to be a slight bias toward higher concentrations of chloride from the right arm compared with the left arm, but this difference is not medically significant.

Adolescent↗

PubMedDate not supplied

The English sweating sickness, with particular reference to the 1551 outbreak in Chester.

During the 15th and 16th centuries in England, there were five epidemics of a disease characterized by fever and profuse sweating and associated with high mortality. This disease became known as the English sweating sickness. The first epidemic occurred during 1485 at around the time of Henry Tudor's victory at Bosworth Field, and the last took place during the reign of Edward VI in 1551. The disease tended to occur during the summer and early autumn. The relatively affluent male adult population, particularly the clergy, seemed to suffer the highest attack rates, and, except in one epidemic, the disease appears to have attacked only individuals native to England. Despite the reputation of the English sweating sickness as a disease with a high fatality rate, records of burials and wills in Chester suggest that the 1551 epidemic did not have a marked effect on the demographics of the population. The etiologic agent is still unknown, although an enterovirus seems to this author to be the most likely pathogen.

Disease Outbreaks↗

PubMed1998

A mutation in the cystic fibrosis transmembrane conductance regulator gene associated with elevated sweat chloride concentrations in the absence of cystic fibrosis.

Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) have been shown to cause cystic fibrosis (CF) and male infertility due to congenital bilateral absence of the vas deferens. We report the identification of a 6.8 kb deletion (del14a) and a nonsense mutation (S1455X) in the CFTR genes of a mother and her youngest daughter with isolated elevated sweat chloride concentrations. Detailed clinical evaluation of both individuals found no evidence of pulmonary or pancreatic disease characteristic of CF. A second child in this family with classic CF was homozygous for the del14a mutation, indicating that this mutation caused severe CFTR dysfunction. CFTR mRNA transcripts bearing the S1455X mutation were stable in vivo , implying that this allele encoded a truncated version of CFTR missing the last 26 amino acids. Loss of this region did not affect processing of transiently expressed S1455X-CFTR compared with wild-type CFTR. When expressed in CF airway cells, this mutant generated cAMP-activated whole-cell chloride currents similar to wild-type CFTR. Preservation of chloride channel function of S1455X-CFTR was consistent with normal lung and pancreatic function in the mother and her daughter. These data indicate that mutations in CFTR can be associated with elevated sweat chloride concentrations in the absence of the CF phenotype, and suggest a previously unrecognized functional role in the sweat gland for the C-terminus of CFTR.

Child↗

PubMedDate not supplied

Analysis of methamphetamine in hair, nail, sweat, and saliva by mass fragmentography.

A method for the detection and quantitation of methamphetamine and its major metabolite in hair, nails, sweat, and saliva from habitual users of methamphetamine by mass fragmentography has been developed. Hair and nail samples were washed with water and methanol to remove the external contamination, processed with 0.6M HCl, alkalinized, and extracted with CHCl3/isopropanol (3:1 v/v). Sweat and saliva samples were extracted with methanol. After trifluoroacetyl derivatization, the samples were analyzed by mass fragmentography. Methamphetamine and its major metabolite, amphetamine, were detected in hair, nail, and sweat samples, but methamphetamine alone was detected in saliva samples.

Amphetamine↗