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We present six patients with congenital hemangioma of eccrine sweat glands. In every one the lesion was congenital, clinically angiomatous, painless, and nonsweating, with progressive involution over months. Histologically all specimens showed many dilated capillaries with prominent endothelial cells associated with the eccrine sweat gland coils.
The object of this study was to measure how accurately drinkers report their consumption of alcohol. Twenty-two normal volunteers kept a written record of all alcoholic beverages they consumed in 1 week. During the same period, their actual intake was monitored by the sweat-patch test for alcohol consumption. Only nine subjects (40.9%) reported their alcohol consumption accurately; two (9.1%) overreported their intake, and 11 (50%) underreported their intake. Five (22.7%) of those who underreported their consumption claimed to have drunk no alcohol at all, but elevated ethanol levels in their sweat-patch tests indicated otherwise. These data suggest that self-reported claims concerning alcohol consumption or abstinence should be received with a degree of skepticism, and that greater emphasis should be placed upon objective laboratory tests for the diagnosis of alcohol abuse.
Marstock thermotesting evaluates A-delta- and C-fiber functions. To optimize this method, intraindividual variations of vasodilatation, blood flow and sympathetic activity probably biasing thermotest results were imitated by exogenous stimuli which strongly exaggerated these intraindividual variations. In 20 healthy subjects, warm (WT), cold (CT), and heat-pain (HT) thresholds were determined in the morning at the thenar (th), the volar wrist (wr), and behind the malleolus internus (mi). Thresholds at the thenar and the volar wrist were compared with those during severe sweating induced by Minor's test, and to those measured when sympathetic activity had been increased by the ingestion of a high dose of caffeine (0.5 g). Furthermore, the intraindividual variation of local capillary blood flow and vasodilatation was imitated by a rubefacient liniment (Forapin) applied to the three sites. After a local hyperemisation had been induced thermal thresholds were measured and compared to those measured without any stimulation. Local hyperemia did not influence thermal thresholds significantly. Sweating only lowered cold thresholds at the thenar significantly and only slightly raised warm and heat-pain thresholds at the thenar. Caffeine significantly lowered warm thresholds and raised heat-pain thresholds at the thenar. To conclude, the tested exogenous interferences do not disturb thermal perception markedly, especially when testing is not performed at the thenar, but at the volar wrist and when the testing-procedure and parameters are standardised.
Healthy volunteers without nickel hypersensitivity were given 5.6 mg nickel orally. The nickel concentration was assayed in urine, serum and sauna-provocated sweat from hands and trunk before and after nickel ingestion. The nickel concentration in serum increased in all subjects, and in most cases in urine, but not decisively in sweat.
Mitotic rates (mitotic figures per 10 400X fields) were determined for 115 sweat gland adenomas. The observations were also combined for all lesions within each category of adenoma. The combined mitotic rates of spiradenoma, cylindroma, syringoma, and chondroid syringoma were each less than 1.0. Individual lesions within these categories often lacked mitotic figures. With the exception of 1 chondroid syringoma, none of the individual lesions within these groups had mitotic rates exceeding 2.0. The combined mitotic rates of acrospiroma and hidradenoma papilliferum were 1.6 and 1.52, respectively. Twenty-five percent of the acrospiromas had mitotic rates exceeding 2.0 (maximum 7.5). Mitotic figures were concentrated in specific cell populations, particularly in acrospiromas and chondroid syringomas. The potential for cell division appeared to be reduced or lost in areas of increased cytologic or structural differentiation. A review of the literature indicates that there can be overlap between the mitotic rates of sweat gland adenomas and those of carcinomas.
Characteristics of keratins of five carcinomas of sweat gland origin were immunohistochemically investigated with several antikeratin monoclonal antibodies with differing specificities. Specimens were obtained from two cases of mucinous carcinoma of the skin, two cases of classic type of eccrine adenocarcinoma, and a case of eccrine porocarcinoma. The tumor cells of mucinous carcinoma expressed only simple epithelial keratins. In a case of eccrine adenocarcinoma, simple epithelial keratin 19 was diffusely expressed. The expression of the other simple epithelial keratins was confined to the luminal cells, whereas the remaining tumor cells further expressed stratified epithelial keratins. Eccrine porocarcinoma and a second case of eccrine adenocarcinoma did not express simple epithelial keratins, although stratified epithelial keratins were diffusely expressed. These data suggest that carcinomas of sweat glands express various combinations of simple and stratified epithelial keratins. Development of additional data along these lines may help to further define their classification.
The diagnosis of cystic fibrosis is straight forward if the clinical findings and sweat sodium are considered together. We describe 3 patients where the diagnosis has proved difficult as both the clinical features and sweat sodium have varied between normal and abnormal.
The rhythmic variations in the water evaporation rate (gm-2h-1,) from the dorsal side of the forearm have been studied. The evaporation rate is estimated by calculating the difference between the vapour pressures at two distinct points on a line perpendicular to the evaporative surface. Using autocorrelation technique it is found that the evaporation rate is periodic with a period of around 0.7 s. This value is consistent, at rest as well as prior to profuse sweating in exercise, for all the subjects included in the investigation. During profuse sweating the period becomes slightly longer. It is suggested that the variations in the evaporation rate reflect the periodic activity in the sudomotor nerves.
Human sweat duct cells in primary culture were investigated by voltage-clamp technique. Stimulation with the muscarinic agonist, metacholine (MCh), produced an abrupt transient rise followed by sustained regular oscillations in the transepithelial short-circuit current (Iscc), which in these cells is carried by a mucosal amiloride-sensitive Na+ influx, secondary to a Ca2(+)-activated, voltage-dependent, large K+ shunt across the serosal membrane. The time of latency, the initial transient phase, and the sustained oscillating phase of the MCh-induced Iscc response were demonstrated to be differently affected by changes in temperature, agonist concentration and external Ca2+ supply. From these results a model is proposed for the MCh-induced signal transduction in cultured sweat duct cells, involving a primary intracellular oscillatory Ca2+ mobilization, activated by IPP, sustained by a temperature-regulated external Ca2+ supply, and counter-regulated by cytosolic Ca2+.
Forearm sweat production rate (SPR) and external auditory meatal temperature (TEAM) were examined in five young and five middle-aged women in response to intermittent exercise, on three separate occasions. The first experiment was a control study, while in the second study the left hand was immersed in cold water at the onset of sweating during each exercise bout, and in the third study this immersion was accompanied by venous occlusion of the upper left arm. TEAM increased by 0.5 degrees C during exercise with no significant differences between the groups on any occasion. The young women displayed a greater peak SPR during exercise in the control than the middle-aged women (52.5 +/- 23.9 vs. 16.7 +/- 6.5 mg cm2 h-1, P less than 0.001). With hand immersion, peak SPR was depressed to 14.0 +/- 4.6 mg cm2 h-1 (P less than 0.001) in the young women and to 13.1 +/- 4.5 mg cm2 h-1 in the middle-aged (P less than 0.05). With hand immersion and venous occlusion the peak SPR in young women increased (43.0 +/- 9.2 mg cm2 h-1). In the older women SPR was 14.9 +/- 6.1 mg cm2 h-1, which was not different from either control or cold-immersed values. Thus, forearm SPR during low-intensity intermittent exercise is greater in young compared with middle-aged women, despite similar changes in TEAM. The response to hand immersion in cold water was more marked in the young subjects.
The changes in cytoplasmic free calcium ([Ca2+]i) which occur in isolated human sweat glands during cholinergic stimulation have been studied indirectly by monitoring potassium permeability. The acetylcholine-evoked permeability increase normally consists of transient and sustained phases which are attributed to the mobilization of intracellular calcium stores and to calcium influx respectively. Such consistent responses to acetylcholine could not be obtained during superfusion with bicarbonate-free, HEPES-buffered solutions. The human sweat gland in vitro therefore appears to have a strict requirement for bicarbonate. The sustained component of the response was not affected by total removal of external sodium, suggesting that calcium influx does not occur via a sodium-dependent system. The transient component, however, was abolished when external sodium was replaced by N-methyl-D-glucammonium (NMDG+). It therefore appears that secretagogue-evoked mobilization of cytoplasmic calcium is dependent, in some way, upon external sodium. This dependence is not, however, absolute as the response was essentially normal when sodium was replaced by lithium.
We have explored the factors that may regulate membrane permeability in a cell line (NCL-SG3) derived from the human sweat gland epithelium. Ionomycin increased the rate of 125I-efflux from preloaded cells and this action appeared to be due to an increase in intracellular free calcium ([Ca2+]i). The ionomycin-evoked increase in 125I- efflux was reduced in cells that were exposed either to barium or to valinomycin in the presence of a high concentration of external potassium. It thus appears that a fraction of the ionomycin-evoked increase in 125I- efflux is due to the activation of potassium channels and experiments using 86Rb+ also suggested that ionomycin increased the rate of potassium efflux, an effect which was totally abolished by barium. Blockade of Na(+)-K(+)-2Cl- cotransport and of Cl- -HCO3- exchange reduced the basal rate of 125I- efflux and the ionomycin-evoked increase in 125I-efflux from control cells and from cells depolarized by valinomycin. These transport systems thus contribute to anion efflux, although [Ca2+]i-dependent chloride channels also appear to be present. Acetylcholine increases [Ca2+]i in the secretory cells of human sweat glands, but this neurotransmitter did not increase [Ca2+]i in NCL-SG3 cells and so membrane permeability was not under cholinergic control. Adrenaline did not increase [Ca2+]i, but this hormone did evoke cyclic-3',5'-adenosine monophosphate (cyclic AMP) production. However, membrane permeability was not under adrenergic control, as the cells did not appear to express functional, cyclic AMP-dependent anion channels. This may be because they were not fully differentiated under the culture conditions. ATP consistently evoked a dose-dependent increase in anion efflux that appeared to be mediated by [Ca2+]i. The increase in [Ca2+]i was initiated by the release of calcium from a limited internal store and was subsequently sustained by calcium influx. UTP and ADP also increased [Ca2+]i, whereas adenosine, AMP and alpha,beta-methylene ATP were without effect. These data thus suggest that a subclass of type 2 purine receptor, which is functionally coupled to phosphoinositidase C, is present in these cells.
1. Using a sensitive method for detecting and monitoring sweat secretion, a study has been made of the effects of adrenaline and noradrenaline on the cat's pad sweat gland activity in the anaesthetized cat.2. Intravenous or intra-arterial injections of adrenaline or noradrenaline only very occasionally caused these glands to secrete.3. The predominant effect of these drugs on glands which are already secreting in response to plantar nerve stimulation is inhibitory.4. The catecholamine inhibition could be reduced or blocked by phentolamine, but not by propranolol, dibenamine or phenoxybenzamine.5. It is concluded that these glands can be directly activated by intravascular injections of adrenaline or noradrenaline, but that the inhibitory effect of concomitant vasoconstriction usually prevents a response being detected at the skin surface.
1. The effects of blocking agents on the responsiveness of the cast' pad and human forearm sweat glands have been studied.2. Of the anti-adrenergic substances examined (dibenamine, phenoxybenzamine, bretylium, guanethidine and phentolamine) only high doses of guanethidine and phentolamine produced any consistent and significant measure of blockade, and small doses of atropine were as effective as these large doses of guanethidine or phentolamine.3. It is concluded from the blockade of chemical stimulation as well as transmission by these substances that (1) there are only cholinergic fibres innervating eccrine sweat glands, and (2) any inhibitory action by anti-adrenergic substances is due to interaction with cholinergic receptors in the glands.
1. Electrophysiological properties and dye-coupling status of secretory, myoepithelial and coiled duct cells in isolated human eccrine sweat glands have been assessed by single-micro-electrode studies and intracellular micro-iontophoresis of the fluorescent naphthalimide dye Lucifer Yellow CH (molecular weight 457). Treated glands were embedded in LKB HistoResin and examined by transmission fluorescence microscopy, first as wholemounts and then as 5 microns serial sections. Sections positive for Lucifer Yellow were photographed and then stained with Toluidine Blue for observation by conventional microscopy to confirm the site of penetration. 2. Out of forty-five successful micro-iontophoreses, three were confirmed in secretory cells, twelve in myoepithelial cells and thirty in cells of the coiled duct wall. The latter were identified as the most penetrable in the coiled part of the isolated human eccrine sweat gland. 3. Of the three secretory cells labelled (resting potentials -40, -52 and -63 mV), all demonstrated dye coupling to neighbouring secretory cells although in one case this was found to be selective. Not every secretory cell was involved in coupling. No fluorescent label spread to the myoepithelial cells which form a network on the basal surface of the secretory tubule. 4. When myoepithelial cells were penetrated, they demonstrated dye coupling to neighbouring myoepithelial cells but not to secretory cells with which they also made contact. Basal resting potentials of -35 to -65 mV were recorded (mean = -52 mV, S.E. of mean = +/- 2.4 mV, n = 12) and, in eight out of the twelve cells penetrated and labelled, spontaneous depolarizing transients were also observed whose amplitude but not frequency increased with increasing membrane polarization. Administration of acetylcholine to produce a final concentration of 10(-6) to 10(-7) M produced either depolarization or micro-electrode dislodgement. 5. Of the thirty cells labelled in the coiled duct, twenty-six showed obvious dye spread to neighbouring cells in both layers of the wall. There was no relation between dye-coupling status and basal resting potential which lay in the range -40 to -82 mV (mean = -60 mV, S.E. of mean = +/- 2.4 mV, n = 30). Repeated doses of acetylcholine produced either no response from cells in this range or depolarization in cells with resting potentials more negative than -70 mV and hyperpolarization in cells with resting potentials more positive than -70 mV. In addition, there was a biphasic response, depolarization followed by hyperpolarization in a cell of resting potential -67 mV.(ABSTRACT TRUNCATED AT 400 WORDS)
1. Isolated coiled reabsorptive sweat ducts from normal subjects and patients with cystic fibrosis (CF) were cultured in vitro. Cells were harvested and plated onto permeable supports to form confluent cell sheets. The Ussing chamber technique was used to study pharmacological regulation of the transepithelial ion transport in these membranes. 2. Addition of a stable cyclic AMP analogue, 8-Br-cyclic AMP, to normal cell cultures resulted in a decrease of the transepithelial potential difference (PD). 3. Forskolin exposure resulted in a similar PD decrease, which was augmented by the phosphodiesterase inhibitor, isobutylmethylxanthine (IBMX). 4. Exposure to isoprenaline, prostaglandin E2 (PGE2), and phenylephrine resulted in a response mimicking the forskolin-induced response, that was also amplified by IBMX. 5. Pre-incubation with cholera toxin abolished the isoprenaline response and reduced the control resistance. 6. Propranolol abolished the responses induced by isoprenaline and phenylephrine, whereas phentolamine had no effect. PGE2-induced responses were inert to both types of blockers. 7. Indomethazine addition to an unstimulated membrane resulted in a weak PD increase, i.e. a response opposite to that induced by isoprenaline. 8. IBMX addition to an unstimulated membrane resulted in a weak isoprenaline-like response. When the cells were pre-treated with indomethazine this IBMX response was absent. 9. Unidirectional Cl- isotope flux studies demonstrated a large increase of net Cl- reabsorption in response to isoprenaline and PGE2. 10. Mannitol isotope flux studies revealed that the paracellular permeability was unaffected by isoprenaline exposure. 11. Membranes derived from CF patients did not respond similarly to any of these agents. However, a weak spike, occasionally followed by a gradual increase of the short-circuit current (Iscc), was observed in both normal subjects and CF patients. 12. It is concluded that the primary effect on ion transport of factors increasing the cyclic AMP in normal cultured sweat duct cells is an activation of a transcellular Cl- permeability. This effect was missing in cells derived from CF patients.
1. The ionic mechanism involved in Ca(2+)-stimulated electrolyte transport in cultured equine sweat gland epithelial cells was studied using the short-circuit current (ISC) technique. 2. Microscopy revealed that the cultured cells grown on Millipore filters formed polarized monolayers with tight junctions. Monolayers exhibited a mean transepithelial resistance of 333.9 +/- 40.4 omega cm2. 3. Ca(2+)-mobilizing agents, A23187 (1 microM) or thapsigargin (0.01-1 microM), stimulated ISC while forskolin exerted little effect on the ISC. 4. Replacement of external Cl- by gluconate significantly reduced the ISC by 63% when stimulated by 0.1 microM thapsigargin. Residual ISC could be abolished (> 99%) by elimination of HCO3- from the bathing solution. 5. Basolateral addition of bumetanide (0.1 mM), ouabain (0.01 mM) and acetazolamide (45 microM) and apical addition of methyl isobutyl amiloride (MIA, 1-100 microM) all had inhibitory effects on the thapsigargin-stimulated ISC to various extents. 6. Substantial current inhibition could be obtained using 4, 4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) and diphenylamine-2-carboxylate (DPC) in a concentration-dependent manner. 7. The K+ channel blocker barium (5 mM) was effective on both sides of the epithelium with a much larger effect on the basolateral side. 8. The inhibitory effects of acetazolamide, amiloride, MIA, DIDS and DPC on the thapsigargin-stimulated ISC were also observed when a Cl(-)-free solution was used. 9. The results provide evidence for Ca(2+)-stimulated HCO3- as well as Cl- secretion by equine sweat gland epithelium.
1. Anion secretion induced by capacitative Ca2+ entry through apical and basolateral membranes of cultured equine sweat gland epithelium was studied using the short-circuit current (Isc) technique. 2. Thapsigargin induced an increase in Isc that could be inhibited when external Ca2+ was chelated by EGTA. 3. The inhibition of the thapsigargin-induced Isc could be reversed by re-addition of Ca2+ to apical or basolateral solutions. The magnitude of the reactivated Isc depended predominantly on basolateral Ca2+ concentration. 4. The magnitude of the reactivated Isc upon basolateral Ca2+ addition increased with the thapsigargin concentration, indicating its dependence on the emptied state of the Ca2+ store induced by thapsigargin. 5. The thapsigargin-induced Isc, as well as the Ca(2+)-dependent reactivation of Isc in EGTA-treated epithelia, was inhibitable by apical, but not basolateral, addition of flufenamate, and by basolateral addition of La3+. Other Ca2+ channel blockers, verapamil and nifedipine, had no effect when applied to either membrane. 6. The results suggest that thapsigargin-induced anion secretion by the equine sweat gland epithelial cells is crucially dependent upon the Ca2+ influx occurring primarily through the basolateral membrane, and that apical and basolateral membranes may possess different pathways for Ca2+ entry.