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Proliferating cells in human eccrine and apocrine sweat glands.

Morphological observations of sweat glands showed degenerated debris of secretory cells in the secretory lumen in both apocrine and eccrine sweat glands. This suggested that dead secretory cells of human eccrine and apocrine sweat glands were released into the lumen and replaced by other cells. However, we did not know which type of cells replaced lost secretory cells. Therefore, we studied the proliferating cells in human eccrine and apocrine sweat glands by labeling S-phase cells in vitro with 5-bromo-2'-deoxyuridine (BrdUrd) and by immunostaining proliferation-associated proliferating cell nuclear antigen (PCNA) with anti-PCNA monoclonal antibody. BrdUrd and anti-PCNA antibody labeled a few secretory cells in eccrine and apocrine sweat glands, but neither method labeled myoepithelial cells. Luminal and peripheral cells of the eccrine and apocrine coiled duct were labeled with both BrdUrd and PCNA. However, we could not find any highly proliferative germinative cells in coiled ducts. Our results suggest that lost secretory cells could be replaced by proliferation of secretory cells themselves rather than by proliferation of myoepithelial cells or duct cells.

Apocrine Glands↗

Sweat gland reactivity to local thermal stimulation in dysautonomia.

An attempt has been made to elucidate the cause of hyperhidrosis in dysautonomia by testing sweat gland responsiveness to local application of heat. Heat was applied to the volar surface of the forearm with temperatures of 41.5 C and less for one to ten minutes. For each subject, the minimal duration of heating at the lowest temperature capable of evoking sweating was determined (threshold). Thresholds were significantly lower in all subjects with dysautonomia. Since one control subject, the father of a dysautonomia subject, had the highest threshold, these tests do not permit detection of the heterozygote. A reasonable explanation for enhanced sweating reactivity to local heat application is an increased excitatory state of reflex centers. These patients appear permanently on the verge of generalized sweating likely to result from minimal additional stimulation.

Adolescent↗

pH of sweat of patients with cystic fibrosis.

pH of the sweat from patients with cystic fibrosis and in controls was measured as a function of the sweat-rate using a fluorescence-pH-indicator (umbelliferone). In both populations sweat is acid at low sweat-rates and alkaline at high ones. The results do not favour an abnormality of the ductal H+-secretion as the pathomechanism of cystic fibrosis.

Bicarbonates↗

[Adenoid cystic sweat gland carcinoma. A clinicopathologic and immunohistochemical study].

Adenoid cystic carcinoma of the skin is one of the rarest sweat gland tumours. We have studied two cases of adenoid cystic sweat gland carcinoma clinically, histologically and immunohistochemically. One tumour was located on the occiput of an 18-year-old male patient, while the other developed on the back of a 49-year-old woman. Histologically, both carcinomas were characterized by basaloid tumour cells showing the typical adenoid-cystic growth pattern. The cells were arranged in solid, cribriform, tubular and cystic aggregates, which were surrounded by mucoid, Alcian blue material. Immunohistochemically, the tumour cells showed coexpression of cytokeratins typical of stratified epithelia (CK1/5/10/14) and cytokeratins of the simple epithelial type, namely CK7, CK8, CK18, and CK19. Coexpression of these cytokeratins is usually observed in normal fetal sweat glands, but not in adult sweat glands.

Adolescent↗

Instrumentation of a handy microscopic probe for concurrent observation and measurement of active sweat secretion, and its applications.

Instrumentation for the concurrent, dynamic monitoring of active sweat glands and perspiration volume is described. A device for the measurement of the rate of sweat secretion was installed on the head part of a microscope. The combined apparatus (microscopic probe) is handy for use and its weight is very light (ca. 300 g). The microscopic probe is easily attached to the surface of human skin. The dynamic activities of the sweat glands on the forehead and nose and under the nose were observed and measurement when thermal, mental and physical stimuli were applied. The activities of individuals sweat glands were asynchronous when observed in units of a few seconds or less; however, they worked synchronously in a unit period of several seconds. The latter were recorded as fine peaks by a strip chart recorder. The proposed system may be useful for the study of the sympathetic nervous system, the skin sympathetic reflex and the working of sudomotor nerves.

Adult↗

Is salt reabsorption in the human sweat duct subject to control?

There is a time lag between the beginning of sweat secretion and fully effective production of fluid of minimum salt content. It is suggested that changes in permeability to water or electrolytes have to be effected and may account for the time lag. The composition of thermal and pilocarpine sweat indicates that pharmacological stimulation does not wholely reproduce the physiological mechanism: pilocarpine sweat contains more sodium and more cyclic AMP, irrespective of the secretory rate. The sweat obtained from patients with cystic fibrosis has been compared with that from normal children: the concentrations of cyclic AMP and cyclic GMP are the same. Defective sodium reabsorption in the patients is therefore unlikely to be due to inadequate or excessive synthesis of these cyclic nucleotides.

Absorption↗

Effects of training, environment, and host factors on the sweating response to exercise.

Because metabolic heat production is proportional to the amount of work performed, the differences in core body temperature (Tcore) of humans exercising at similar absolute exercise intensities are due to differences in their efficiency of heat dissipation. The purpose of this paper is to delineate the effects of training status, heat acclimation, environmental conditions and host factors on the sweating response to exercise. These factors are reviewed in light of their effects on the biophysical enhancement or suppression of sweating, and modifications of the relationship between local sweat rate and Tcore (degrees C). Athletes are advised to optimize those factors that enhance, and eliminate those factors that diminish, the onset and responsiveness of sweating.

Acclimatization↗

Sweat responses in the aged.

The sweating responses to thermal stimulation and to the intradermal injection of acetyl choline or methacholine were measured in 28 men and 18 women aged 70 and over and were compared with the responses in young control subjects of both sexes. There was found to be a marked reduction in the sweating activity of the majority of aged men in comparison with the younger age groups and the body temperature threshold for the onset of sweating was increased. The reduced response and elevated threshold were even more pronounced in aged females. There is considerable variability in response in different subjects and at different bodily sites. Impairment of thermoregulatory function due to diminished or absent sweating is thought to be one of the factors responsible for increased mortality in the elderly population during heat-waves.

Acetylcholine↗

Sweat gland disturbances in granuloma annulare and necrobiosis lipoidica.

We studied sweat gland distribution, density and activity in thirteen cases of granuloma annulare and ten cases of necrobiosis lipoidica, using a combination of the plastic impression and starch-iodine methods. The pattern of sweat gland disturbance in the two diseases was entirely different. In necrobiosis lipoidica an intense and uniform hypohidrosis was detected throughout the lesion, whereas in granuloma annulare the disturbance followed the morphology of the lesion (the papular border showed complete anhidrosis, whereas the flat central part of the lesion showed only moderate hypohidrosis or normal sweating). The method assigns numerical values to the 'relative density' and the 'relative activity' of the functioning sweat glands compared with normal skin, thus permitting statistical evaluation of the results.

Adolescent↗

The effects of thermal stimulation on the ultrastructure of the human atrichial sweat gland. I. The fundus.

Ultrastructural examination of sweat glands from the human loin before and during heat-induced activity indicated that the sweat is formed from the contents of disrupted cells as well as from the products of secretion. The principal secretory processes appear to be fluid transport and exocytosis of vesicles. However, configurations suggesting microapocrine secretion were also observed. It is concluded that the mechanisms involved in sweat production in man are fundamentally similar to those in animals and the terms 'apocrine' and 'eccrine' should be discarded. The myoepithelial cells which were contracted at the onset of sweating appeared to be under less tension after 3 h of continuous activity.

Adult↗

Lectin-binding sites in eccrine sweat gland tumours.

Lectin-binding sites in sections of formalin-fixed, paraffin-embedded eccrine sweat gland tumours were investigated using fluorescein isothiocyanate (FITC) conjugated peanut agglutinin (PNA), FITC conjugated Ricinus communis 1 agglutinin (RCA-1) and FITC conjugated wheat germ agglutinin (WGA). In 22 benign eccrine sweat gland tumours, lectin-binding sites were noted primarily on the cell surface, and in the secretions. In five malignant sweat gland tumours, all showed cytoplasmic lectin-binding sites in variable proportions of malignant cells in addition to cell surface staining. These results indicate that cytoplasmic lectin-binding sites may be a useful marker of neoplastic transformation of eccrine sweat gland tumours.

Cell Membrane↗

Vasoactive intestinal peptide (VIP) and peptide histidine methionine (PHM) in human eccrine sweat glands: demonstration of innervation, specific binding sites and presence in secretions.

Vasoactive intestinal peptide (VIP) and peptide histidine methionine (PHM) immunoreactivities have been detected in alcohol extracts of human axillary skin using sensitive and specific radioimmunoassays. VIP immunoreactivity (7.63 + 2.33 pmol/g, x + SE, n = 9) was more abundant than PHM immunoreactivity (3.86 + 0.56 pmol/g, x + SE, n = 9). Immunocytochemistry of sections of skin revealed a network of VIP/PHM immunoreactive nerve fibres around the perimeter of eccrine but not apocrine sweat glands. In vitro autoradiography of skin sections using 125I-labelled VIP and PHM, demonstrated binding sites on the membranes of eccrine gland secretory cells. The binding of each radiolabelled ligand was eliminated by the presence of a large molar excess of appropriate cold peptide but was unaffected when incubated with related peptide, indicating the presence of specific binding sites for both VIP and PHM. Radioimmunoassay of Sep-pak concentrated human sweat identified the presence of both VIP immunoreactivity (30.6 pmol/l) and PHM immunoreactivity (43.4 pmol/l). Reverse-phase HPLC analysis of axillary skin extracts and sweat, followed by radioimmunoassay of fractions, identified single resolved peaks of VIP and PHM immunoreactivity with identical retention times to synthetic standards. Eccrine sweat glands in human axillary skin have VIP and PHM peptidergic innervation and possess specific binding sites for each peptide which are both secreted to the surface of the skin.

Binding Sites↗

The relationship of sweat gland count to electrodermal activity.

This study assessed whether greater skin conductance activity at the distal versus medial site (Scerbo, Freedman, Raine, Dawson, & Venables, 1992) is attributable to a greater number of active (open) sweat glands at the distal site. The number of sweat glands was measured using the Palmar Sweat Index (PSI). Twenty-four subjects were exposed to 10 auditory stimuli. Electrodes were placed on the fore and middle fingers of each hand, using distal sites on one hand and medial sites on the other. The PSI was measured at the medial and distal phalanges adjacent to the electrode placement sites. The distal site contained more open and total sweat glands. Open gland count had the strongest correlations with skin conductance. Multivariate analyses of covariance revealed that site effects for nonspecific and orienting response frequency and trials to habituation were associated with site differences in open glands. Skin conductance measures and the PSI reveal greater electrodermal activity at the distal site. In addition, the number of open glands may be a useful measure related to electrodermal response frequency when polygraph measurement is unavailable.

Acoustic Stimulation↗

Immunohistochemical markers of sweat gland tumors.

Using immunoperoxidase methods, normal sweat glands, 44 benign and 4 malignant sweat gland tumors were tested for the presence of carcinoembryonic antigen (CEA), pregnancy-specific-B1-glycoprotein (SP1) and actin (ACT). CEA and SP1 stained the secretory and duct-lining cells of normal eccrine glands. Among benign tumors, 74% were positive for CEA and 44% for SP1. The staining reaction was found mainly in luminal secretions and surrounding cells. Staining by SP1 was reduced, but not suppressed, after absorption with the purified antigen. ACT was found in myoepithelial cells of the secretory tract of normal glands and in basal cells of all cases of hidradenoma papilliferum. Only 3 sweat gland carcinomas reacted for CEA. In a malignant chondroid syringoma, no ACT-positive cells were seen in the myxochondroid stroma. The potential value of CEA, SP1 and ACT in the diagnosis of sweat gland tumors is discussed.

Actins↗

Activity of the human eccrine sweat gland during exercise in a hot humid environment before and after acclimatization.

1. Six unacclimatized African mine labourers were subjected to exercise for 4(1/2) hr in a hot humid environment (90 degrees - 93 degrees F wet-bulb/dry-bulb (W.B./D.B.); approximately 90% r.h.) 2. The patterns of glandular activity and the densities of active glands on the chest and back were assessed half-hourly from plastic impressions. Acclimatization increased and prolonged glandular activity. The increment in activity of the sweat glands on the back was greater than that on the chest. 4. There was no significant increase in the maximum number of active glands on either site after acclimatization. 5. Acclimatization greatly reduced the number of inactive glands, subsequent to the maximum count, on the back, but this was not observed on the chest. 6. The increased sweat rates with acclimatization were due mainly to increased glandular activity. 7. The decline in sweat rates and activity on prolonged exposure to hot humid environment was attributed to glandular fatigue. Other factors, such as increased body temperature, hydration of the skin and fatigue of the central nervous system, suggested by other investigators as possibly causing the decline in sweat rates, did not have support in this study.

Acclimatization↗

A comparison of sweat gland activity in eight species of East African bovids.

1. The pattern and control of the sweat glands of eight species of wild bovids has been studied.2. Heat exposure resulted in changes in cutaneous moisture loss which showed considerable species variation. Duiker, Grant's gazelle, Thomson's gazelle and oryx all demonstrated periodic discharges of moisture on to the surface of the skin. Defassa waterbuck and eland exhibited discharges which were accompanied by a gradual rise in basal level. Buffalo showed an immediate large increase which was sustained during the period of heat exposure. Three wildebeest displayed small fluctuations whilst a fourth animal showed a step-wise increment in cutaneous moisture loss.3. The intravenous infusion of adrenaline into the buffalo and one wildebeest caused an increase in cutaneous moisture loss, the magnitude of which was directly related to the size of the dose administered. In three other wildebeest, and all other animals tested, a single injection of adrenaline was necessary to cause a discharge of moisture on to the surface of the skin. Noradrenaline was without effect.4. Heat-induced but not adrenaline-induced sweating was inhibited by the intravenous administration of an adrenergic neurone blocking agent, bethanidine.5. It is concluded that the sweat glands of the wild bovids studied are under adrenergic neurone control, in common with the domestic bovids previously studied, and that there is no correlation between the pattern of sweating and the phylogenetic position of the species.

Animals↗

Sodium transport: inhibitory factor in sweat of patients with cystic fibrosis.

A factor inhibitory to sodium transport exists in the sweat of patients with cystic fibrosis of the pancreas. When the duct system of the rat parotid was perfused with sweat from patients, marked inhibition of sodium reabsorption was observed. Perfusion with sweat from normal subjects caused no change in sodium reabsorption. The factor thus demonstrated may be responsible for the increased sodium concentrations in the sweat of patients with cystic fibrosis.

Absorption↗

Regional rates of sweat evaporation during leg and arm cycling.

The rate of sweat evaporation from the arm, chest, back and thigh, aural temperature, skin temperature (arm, chest, back and thigh), heat production (derived from measurements of respiratory gas exchange) and heart rate were measured in 7 men during 15 minutes of leg or arm cycling at 32% of predicted maximum oxygen uptake (VO2 max). The regional sweat evaporation rates and changes in body temperature were similar during both forms of exercise. The peak rates of sweat evaporation from the arm, chest, back and thigh were 15.7 +/- 19.8, 25.0 +/- 21.6, 28.7 +/- 22.7 and 21.0 +/- 18.2 mg.cm-2 hr-1 during leg cycling and 13.2 +/- 11.6, 22.2 +/- 14.4, 27.6 +/- 14.7 and 19.2 +/- 13.3 (SD) mg.cm-2 hr-1 respectively during arm cycling. The sweat evaporation rates from the different body regions were not significantly different from one another.

Adult↗