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Innervation of sweat glands in the forehead. A study in patients with Horner's syndrome.

The amount of sweating in lateral and medial sites in the forehead was investigated with quantitative evaporimetry in 18 patients with Horner's syndrome: eight cases with a central (1st), five with a preganglionic (2nd), and five with a postganglionic (3rd) neurone lesion. The amount of sweating was measured after body heating, and, at another occasion, after intracutaneous injection of the cholinergic drug pilocarpine. The two sites were at the root of the nose (medial position) and at the lateral angle of the eye (lateral position). Generally, there was a reduced level of sweating on the symptomatic versus the non-symptomatic side in both positions during body heating, except in the lateral part of the forehead in the 3rd neurone lesions, where sweating was greater on the symptomatic than on the non-symptomatic side. There was a nearly symmetrical sweating response after pilocarpine injection at all sites. There was one exception to this rule; the lateral position in the preganglionic neurone lesion group where pilocarpine induced more sweating on the non-symptomatic side. Thus, the results suggest a relative supersensitivity to pilocarpine in the medial position for all patients and in the lateral position for the central neurone lesion group. The findings suggest that the innervation of sweat glands in the medial and lateral parts of the forehead is different, the medial part being supplied by nerve fibres from the sympathetic plexus of the internal carotid artery, while the sweat glands in the lateral part is furnished from the plexus surrounding the external carotid artery.

Autonomic Fibers, Postganglionic↗

Cutaneous microdialysis as a novel means of continuously stimulating eccrine sweat glands in vivo.

Previous studies of the pharmacological regulation of sweat gland function in humans have administered agonists or antagonists systemically, by local intradermal injection or by iontophoresis. This has not allowed prolonged or steady-state activation of sweat glands to be examined. In this study, we used the technique of dermal microdialysis to administer pharmacological agents singly and in combination for up to 5 hours. Muscarinic stimulation with pilocarpine nitrate (50 mug ml(-1) to 1.66 mg ml(-1)) produced a sigmoid dose response curve, with maximal sweating (measured as transepidermal water loss) (mean 70 g m(-2) hour(-1)) after 15 minutes. This was sustained at steady-state levels (55 g m(-2) hour(-1)) until perfusion stopped. Perfusion with atropine (0.003 mg ml(-1)) reduced sweating below baseline and blocked pilocarpine-induced sweating completely. Noradrenaline (0.005 mg ml(-1)) induced much lower sweat rates than pilocarpine (56.8+/-1.62 g m(-2) hour(-1) vs 8.2+/-1.2 g m(-2) hour(-1), respectively, P<0.001) and this was unaffected by co-administration of atropine. This method has made it possible to show that sweat glands are capable of sustaining near maximal activity for at least 5 hours. The method has future application in investigation of conditions with disordered sweat gland activity.

Adrenergic alpha-Agonists↗

Circadian variation of sweating responses to passive heat stress.

The aim of present study was to examine whether sweating responses to passive heat stress change with the circadian rhythm of internal temperature. Six men had their legs immersed in water at 42 degrees C for 60 min in an ambient temperature of 28 degrees C on four separate days. Experiments were conducted at four different times [06.00 h (morning), 12.00 h (daytime), 18.00 h (evening) and 24.00 h (night)]. We measured oesophageal temperature (Toes), mean body temperature (Tb), local sweating rate (msw) on the forehead, back, forearm and thigh, the densities of activated sweat gland (ASG) on the back, forearm and thigh, and the frequency of sweat expulsion per minute (Fsw) which has been suggested to represent central sudomotor activity. Sweat gland output (SGO) on each site was calculated by dividing msw by ASG. ASG was significantly higher on the forearm than on the back and thigh, and SGO was significantly lower on the forearm than on the back and thigh. However, ASG and SGO did not significantly change over the day. Tb and Toes thresholds for the onset of sweating showed a significant change with both the temperature rhythms at rest prior to each procedure, while the slopes of the relationships Fsw-Tb and msw-Fsw showed no significant difference over the day. We suggest that the circadian variation of sweating response to passive heat stress is regulated by a central sudomotor mechanism rather than by sweat gland function.

Adult↗

Cathelicidin anti-microbial peptide expression in sweat, an innate defense system for the skin.

The eccrine gland is one of the major cutaneous appendages and secretes sweat. Its principal function is thermoregulation during exposure to a hot environment or physical exercise. In addition to this function, we show that LL-37, a member of cathelicidin family of anti-microbial peptides, is expressed in sweat. LL-37 protein and mRNA was seen in the eccrine structures of normal human skin by immunohistochemistry and in situ hybridization. LL-37 was localized to both the eccrine gland and sweat ductal epithelial cells, whereas dermcidin, a previously described natural antibiotic in sweat, was expressed only in the gland itself. The anti-microbial activity of LL-37 and dermcidin against various bacteria in the sweat ionic environment was demonstrated by solution colony forming assay using synthetic peptides, and in sweat obtained from normal volunteers. These results indicate that cathelicidin is secreted in human sweat, has potent anti-microbial activity against both gram-positive and gram-negative bacteria, and can, after processing from the preproform, provide a barrier for protection against infection. Thus, sweat represents a unique mode of delivery for potent innate immune effector molecules in the absence of inflammation.

Amino Acid Sequence↗

The pattern and control of sweating in the sheep and the goat.

1. The pattern and control of sweating in one breed of goat and six breeds of sheep have been studied.2. Heat exposure of both sheep and goats resulted in periodic discharges of moisture on to the surface of the skin of the shorn mid-side. The frequency of discharge showed considerable variation between individual animals, varying from less than 1/hr to 14/hr. Approximate counts of the number of active sweat glands suggested that the same glands were involved at each discharge.3. The amount of moisture produced at each discharge declined upon continued heat exposure. The rate of decline was independent of the frequency of discharge.4. Adreno-medullary denervation had no effect on the pattern of sweating in either the sheep or the goat.5. Intravenous adrenaline administration (5 mug/kg body wt.) caused the sweat glands to discharge, but noradrenaline had no effect at the same dose.6. Thermal sweating was inhibited by bethanidine and phenoxybenzamine but not by propranolol. Sweating induced by intravenous adrenaline administration was blocked by phenoxybenzamine but not by bethanidine or propranolol.7. It is concluded that sweating on the mid-side of the sheep and goat is controlled by an adrenergic mechanism, that secretion from the adrenal medulla under conditions of mild heat stress does not stimulate the glands and that sweating is mediated by adrenergic alpha-receptors.

Adrenal Medulla↗

Individual variations in structure and function of human eccrine sweat gland.

The mechanisms underlying variations in perspiration rate at the glandular level are still poorly understood. Human eccrine sweat glands were dissected from the back of 12 adults, cannulated, and stimulated in vitro with methacholine (Mch). The maximal sweat rate and pKA for Mch determined from the dose-response curve for each individual were compared with the anatomic dimensions of the isolated secretory tubules. There was significant correlation between Mch sensitivity (pKA) and the size of the sweat gland, sweat rate per gland, sweat rate per unit length of the secretory tubule, and sweat rate per unit glandular volume. The sweat glands from individuals judged to be poor sweaters exhibited smaller size, lower secretory activity both in vivo and in vitro, and decreased Mch sensitivity compared with glands from physically fit individuals. We conclude that the increased Mch sensitivity and glandular hypertrophy are the two important features of functionally active sweat glands and infer that these parameters could improve as a result of acclimatization to physical exercise and/or heat.

Adult↗

Effect of physical training on peripheral sweat production.

The purpose of this study was to determine the in vivo secretory activity of sweat glands from sedentary and trained subjects. Peripheral sweat production was determined using pilocarpine iontophoresis in 40 volunteers (10 sedentary men, 10 endurance-trained men, 10 sedentary women, 10 endurance-trained women). Peripheral sweat rate was significantly (P less than 0.05) greater in trained men [6.9 +/- 0.6 (SE) g.m2.min-1] and women (6.1 +/- 0.7) compared with sedentary men (3.1 +/- 0.5) and women (2.5 +/- 0.4). Furthermore, peripheral sweat rate was significantly correlated (r = 0.73) with maximal O2 uptake. The above two findings would suggest that physical training improves the secretory activity of the human sweat gland. Such a result supports previous findings that have suggested that the potentiation in sweating seen after training is achieved via a peripheral mechanism. In addition, several gender-related differences were found in the sudorific response of men and women. Specifically, women have a significantly greater sweat gland density, whereas men have a greater sweat production per gland.

Adult↗

Quantification of the response of equine apocrine sweat glands to beta2-adrenergic stimulation.

The aim of the present study was to characterise the quantitative sweating response of the horse to beta2-adrenergic stimulation. The sweating responses of 6 horses to the randomised infusion of 8 different adrenaline concentrations (0.025, 0.05, 0.075, 0.1, 0.2, 0.4, 1.0 or 2.0 microg/kg bwt/min), was investigated. Sweating rate (SR) and skin temperature (TSK) on the neck (N) and gluteal region (G), and plasma adrenaline and noradrenaline concentrations were measured. Peak SR was approximately 15 (N) and approximately 9 g/m2/min (G) during infusion of both 1.0 and 2.0 microg/kg bwt/min adrenaline. Sweat produced per nmol/l plasma adrenaline peaked during the infusion of 0.075 microg/kg bwt/min adrenaline. Higher adrenaline infusion concentrations resulted in a progressive decrease in the amount of sweat produced per nmol/l plasma adrenaline and a plateau of 6 g/m2/(nmol/l) plasma adrenaline was reached for infusions between 1.0 and 2.0 microg/kg bwt/min. Peak SR were far lower than we have previously reported during exercise. There was no evidence of sweat gland fatigue or vasoconstriction during infusion, suggesting saturation of sweat gland beta2 receptors. We conclude that sweating in the horse is under dual control from a combination of hormonal and neural mechanisms.

Adrenergic beta-Agonists↗

[Peptidergic sweating in multiple system atrophy and hereditary spinocerebellar ataxia with special reference to calcitonin gene-related peptide].

Calcitonin gene-related peptide (CGRP)-like immunoreactivity has been demonstrated to be present in nerve terminals around the sweat glands. We have previously demonstrated that CGRP modulates the cholinergic sweating activity. The present study was designed to evaluate the locally administrated CGRP on sweating of patients with multiple system atrophy (MSA) and hereditary spinocerebellar ataxia (HSCA) consisting of 10 males and 11 females. Among 9 HSCA, 3 was diagnosed as Machado-Joseph disease by clinical and DNA diagnostic assessment. CGRP and methacholine chloride (MCH) was dissolved in saline solution to specified concentration, and 0.1ml of which was injected intradermally at the center of a forearm test area. The sweat rate was recorded continuously by the capacitance hygrometry in a relatively cool environment in which the spontaneous sweating was absent. CGRP significantly increased the sweat rate when it was administrated with MCH on normal subjects. There was a clear dose-dependent relationship between the dose of CGRP and its enhancement. This enhancement was significantly reduced in patients with MSA as compared with controls. On the other hand, most of HSCA showed no remarkable impairment of CGRP enhancement. These results suggest that peptidergic sweating is extensively affected in patients with MSA but is not in patients with HSCA, which may be the consequence of peptidergic sweating dysfunction in MSA.

Adult↗

Sweat studies in hyperhidrosis palmaris and plantaris. A survey of 60 patients before and after cervical sympathectomy.

60 patients suffering from excessive sweating in the hands underwent cervical sympathectomy. At follow-up 1-7 years after operation the hands were dry in 55. No differences in electrolyte concentrations were found in the sweat from palms, arms, or body prior to and after the surgical intervention. Similarly no differences were found in electrolyte concentrations between healthy subjects and hyperhidrotics. Palmar sweat was hypertonic in comparison to arm or body sweat. The Na and K sweat concentrations were: palmar 50 +/- 20 and 16 +/- 7 mEq/1; arm 30 +/- 11 and 8 +/- 2 mEq/1; and body 21 +/- 20 and 4 +/- 3 mEq/1, respectively. Na/K ratio was: palmar 3.2; arms 3.6 and body 5.8. Total sweat loss prior to the operation was 5.7 +/- 4.2 g/kg BW/h; afterwards it was 5.9 +/- 4 g/kg BW/h. These equal sweat rates were associated with compensatory sweating in areas of the body not affected prior to the operation.

Adolescent↗

Apocrine sweat glands in the circumanal glands of the dog.

Apocrine sweat glands in the circumanal glands of the dog are not connected morphologically with the lobules of the circumanal glands. However, an apparent functional association has been demonstrated and it is possible that the apocrine sweat glands might serve as excretory ducts for degenerated polyhedral cells of the circumanal glands. In this study, we examined the ultrastructure of the apocrine sweat glands in the circumanal glands of the dog in an effort to define more precisely the relationship between the apocrine sweat glands and the circumanal glands. Paraffin sections stained with azan and sections after immunohistochemical staining with antibodies against actin were examined by light microscopy. Samples fixed by aldehyde perfusion were examined with the electron microscope. Diameters of apocrine sweat glands and height of cells in the secretory epithelium varied considerably. Immunohistochemical staining for actin was weakly positive in the supranuclear regions of secretory cells and very intense in myoepithelial cells. In secretory cells, the endoplasmic reticulum was well-developed. Multivesicular bodies were abundant and were discharged into lumens. Apocrine secretion and exocytosis were observed at luminal surfaces of secretory cells. There were three types of large granule in the cytoplasm: giant mitochondria without cristae; membrane-enclosed globules with or without myelin-like contents; and electron-dense, homogeneous, globular structures. Luminal surfaces were always covered with microvilli, and extensive folding of the cell membrane was found in basal regions. Bundles of actin filaments were dispersed throughout the cytoplasm. In the lumens of apocrine tubules, we observed shed secretory cells with well-preserved normal fine structures. We also noted the differentiation of secretory cells that was due to cell renewal. Apocrine sweat glands in the circumanal glands of the dog appear to be more active than those on the general body surface in terms of apocrine secretion, exocytosis, and the release of multivesicular bodies. Shed secretory cells containing large granules, as well as degenerated polyhedral cells from the circumanal glands, might contribute, to some extent, to the subtle composition of sweat from these apocrine sweat glands.

Animals↗

Serum lipase levels as a diagnostic marker in cystic fibrosis patients with normal or borderline sweat tests.

Patients with normal or borderline sweat test present a diagnostic challenge. In spite of the availability of different methods such as genetic analysis and measurements of nasal potential difference, uncertainty in diagnosing cystic fibrosis (CF) in some patients still exists. Neonates with CF have high serum lipase levels, which decline over time in pancreatic-insufficient patients, whereas pancreatic-sufficient patients demonstrate high serum lipase levels beyond infancy. Because patients with borderline or normal sweat test are almost always pancreatic sufficient, this study was aimed to assess whether serum lipase levels may be of help in establishing the diagnosis of CF in these patients. Serum lipase levels were measured in 100 CF patients and in 17 healthy individuals. Patients were grouped according to their genotype. Group A patients (n = 70) carried two mutations previously found to be associated with a pathologic sweat test and pancreatic insufficiency (delta F508, W1282X, G542X, N1303K, S549R). Group B (n = 30) were compound heterozygote patients who carried one mutation known to cause mild disease with borderline or normal sweat tests and pancreatic sufficiency (3849+10kb C-->T, 5T). Group C included 17 healthy controls. Serum lipase levels ranged between 2 and 104.4 U/L (mean +/- SD 16.9 +/- 14.7), 6.1-200 U/L (mean +/- SD 53.9 +/- 47.9), and 8.5-27.8 U/L (mean +/- SD 16.9 +/- 5.1) in Groups A, B, and C, respectively, with some overlapping between groups. The distribution of lipase levels was significantly different in Group B vs Groups A and C (P < 0.01). High lipase levels were found in 63.3% (19/30) of Group B patients, but in only 4.3% (3/70) and 0% (0/17) of Group A and C, respectively. Lipase levels were found to be inversely related to sweat chloride concentrations (r = -0.19, P < 0.05). Patients with borderline or normal sweat tests had high lipase levels, whereas low lipase levels were associated with pathologic sweat tests. Our findings indicate that the serum lipase level is genetically determined and that it has a useful role in the diagnosis of CF. Thus, in patients with borderline sweat tests and high lipase levels, the diagnosis of CF should be considered.

Adult↗

Modifications of sweating responses to thermal transients following heat acclimation.

The sweating response was studied before and after passive humid heat acclimation in four resting male subjects who were exposed to slow thermal transients increasing air and wall temperatures from 28 degrees C to 45 degrees C. The slopes of the ambient temperature increases were +0.19 degrees C . min-1; +0.16 degrees C . min-1 or +0.14 degrees C . min-1. Dew-point temperature and air velocity were kept constant (17.5 degrees C; 0.3 m . s-1). Continuous measurements were made of oesophageal temperature, mean skin temperature, whole-body sweat loss and of right upper limb sweating responses. The local sweating response was measured from an arm chamber under a local thermal clamp (Tsk,1 = 38 degrees C). The results confirmed the fact that heat acclimation to humid heat induces a shortening in the time lag of sweat onset and increases the local sweating rates while internal temperature changes are reduced. These modifications are interpreted as a non-linearity in the response of the central controller, involving both a change in the central gain and an upward resetting of the "local sweating rate-body temperature" curves, without any shifting of the hypothalamic set-point temperature as it is currently described. However, a modification of local sweat gland activity occurring with heat acclimation cannot be ruled out.

Acclimatization↗

Dynamic sweating response of man to infrared irradiation in various spectral regions.

In an attempt to detect differences in the thermal effect of infrared irradiation of different wave-lengths, transient sweating response to infrared irradiation in various spectral regions was examined. In Series 1, the ventral or dorsal surface of the nude subject was irradiated repetitively for a period of 4 min (2 min on, 2 min off) by each of three kinds of infrared heaters with main emissivity in 'near-infrared' (NIR; 0.7-2.8 microns), 'intermediate-infrared' (MIR; 1.5-5.8 microns), and 'far-infrared' (FIR; 2.8-25 microns) regions. The sweating response on a non-irradiated area tended to be the greatest with MIR, while the magnitude of the sweating response on the irradiated area showed no consistent differences among various wavelengths. The results infer that MIR stimulated cutaneous thomoreceptors most effectively, while its direct effect on local sweat gland activity was minimal. In Series 2, the effects of 9-12 min irradiations in more restricted ranges of wavelength were compared by the combination of the three kinds of heaters with filters (translucent to wavelength ranges of 1.3-2.7, 2.7-3.5, 3.6-8.0 microns, respectively). The sweating response on a remote area was predominantly greater with the range of 2.7-3.5 microns than with the other wavelength ranges, while the local effect on sweating was minimal with this range. The results of Series 2 reinforce those of Series 1, indicating that the degree of stimulation of cutaneous thermoreceptors and of direct thermal effect on sweat gland activity differ with spectral regions incident on the skin, thus affecting local and remote effects on the sweating response.

Adolescent↗

Development of sweating ability in winter- and summer-born Friesian calves aged 1 to 6 weeks.

Sweating rate, rectal and skin temperatures and respiration rate were measured at weekly intervals from 7 days of age (for 4 weeks in Experiment 1; 6 weeks in Experiment 2) in winter- and summer-born Friesian calves exposed to a temperature of 39 degrees C dry bulb and 32 degrees C wet bulb in a climate chamber. Four calves were studied in each season in both experiments. In Experiment 1, ambient temperatures were from 3 degrees to 9 degrees C higher in early summer than in late winter. During each 39 degrees C exposure, sweating rate increased from basal levels of 40-90 to plateau levels of 120-300 g/m2 per h after 90-120 min. The increase in sweating rate with age was most pronounced in winter-born calves, but summer-born calves had higher values at 1 week of age (167 +/- 52.4 vs 94.4 +/- 30.1 g/m2 per h). Seasonal differences in ambient temperature were greater in Experiment 2 (11 degrees to 17 degrees C). In this case summer-born calves had higher sweating rates at each age (plateau values of 220-320 g/m2 per h), and showed a more rapid increase in sweating rate during each 39 degrees C exposure than winter-born calves (plateau values of 100-250 g/m2 per h). The results demonstrate major changes in sweating competence during the first 4-6 weeks of life in Friesian calves, a quite pronounced effect of season (ambient temperature) on the levels of sweating achieved, and indicate that low sweating rates in newborn calves are a contributing factor in deaths due to hyperthermia in semi-arid grazing areas.

Age Factors↗

A new approach to analysis of human sweating.

In human skin transplanted to the back of 3 strains of immuno-deficient mice the function of the eccrine sweat glands of the human transplant was tested by topical intradermal application of pilocarpine, adrenaline and atropine + pilocarpine. Sweat responses were observed in pre-selected fields of observation by means of video macroscope. The iodine starch reaction served as an indicator for the appearance of sweat sport and permitted the evaluation of areas wetted by sweat in the field of observation. Among 9 animals tested, the hybrids between the CB-17-scid mouse and the BALB/cA-nu mouse (BALB/cA-nu,scid) seemed to exhibit the most consistent sweating response to local pharmacological stimulation. According to histological examination, eccrine sweat glands were preserved in human skin transplanted into the back skin of the BALB/cA-nu,scid mouse strain. The heterologous, human skin graft provides a novel model permitting, independent of the normal sweat gland innervation, the analysis of molecular receptors of sweat gland cells by which the actions of natural transmitters and pharmacological agents are transduced.

Animals↗

The mechanism of a human reaction to vibration stress by palmar sweating in relation to autonomic nerve tone.

OBJECTIVES: To clarify the mechanism of a human reaction to vibration stress by palmar sweating in relation to the autonomic nerve tone. METHODS: The autonomic nerve tone was divided into four types by using digital photoelectroplethysmography (PTG) with auditory stimuli: normal (N), hyperreactive (I and D), and hyporeactive (P) types. Palmar sweating and digital PTG were simultaneously measured on the right palm and middle finger, respectively, in 20 healthy men. The left hand gripping the handle with a grasp strength of 49 N was exposed to vibration at a frequency of 125 Hz and acceleration magnitudes of 0 m/s2 (as a control), 30 m/s2, or 50 m/s2 for 3 min. The volume of palmar sweating was recorded before, during, and 30 min after vibration load. Three kinds of drugs related to the autonomic nervous system were orally administered to the subjects. Then 80 min after administration, the experiments were repeated. RESULTS: Of 20 subjects, 17 showed normal autonomic nerve tone (N type), and 3 hyperreactive (I type). The palmar sweating reaction to vibration in I-type subjects was greater and lasted longer than that in N-type subjects. Vibration with an acceleration of 50 m/s2 produced the greatest reaction which was about 7 times larger than that at 0 m/s2 and 2.5 times that at 30 m/s2 (P < 0.01). Sulpiride decreased palmar sweating during vibration, while prazosin and scopolamine inhibited it. CONCLUSIONS: The palmar sweating reaction to vibration stress was related to the background level of the autonomic nerve tone. The sweating volume was in direct proportion to the acceleration magnitude of vibration. The reaction of palmar sweating to vibration stress may be mediated through both the adrenergic and cholinergic fibers of the autonomic nervous system.

Adrenergic alpha-Agonists↗

[Effectiveness of botulinum toxin A in the treatment of gustatory sweating].

Frey's syndrome is present in almost all patients after parotidectomy. Gustatory sweating reduces quality of life. Injections of botulinum toxin A have recently been described as effective. This study was designed to evaluate the efficacy of this new treatment. Nineteen patients with severe gustatory sweating following superficial parotidectomy were treated. One unit/cm2 botulinum toxin A was injected intracutaneously into the affected area once. Minor's starch iodine test was performed to prove the outcome of therapy 4 weeks later. Eight patients lost their sweating. However, another seven patients had some blue spots on their cheeks. In four patients whose sweating had extended beyond the hairline, remnants of gustatory sweating showed up. Overall, the affected area of gustatory sweating could be reduced by botulinum toxin A from an average of 31 cm2 before treatment to 4 cm2 after treatment. Although there were some remnants of sweating in a few patients, Frey's syndrome was gone in all cases. No side effects could be observed. Intracutaneous injections of botulinum toxin A are highly effective and safe in treatment of gustatory sweating.

Adult↗