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PubMed1986

Modulation of the chloride concentration of human sweat by prolactin.

The purpose of this study was to determine whether the availability of PRL modulates the chloride concentration of human sweat. Full thickness human skin grafted into the back of immunoincompetent, nude, congenitally athymic mice heals in about 6 to 10 weeks and survives the life of the mice. Mice have no sweat glands in the back so this system provides a useful model for study of the physiology and pathology of human sweat glands. The graft can be induced to sweat and the sweat collected for analytical studies. Presumably normal skin obtained from 7 individuals undergoing reconstructive surgery was grafted successfully into 11 mice. On 49 occasions sweat was induced by pilocarpine iontophoresis and collected for 45 min. The chloride concentration was 12.9 +/- 6.7 meq/liter, values typical of normal human sweat. Nine mice bearing grafts were injected with rabbit anti-human PRL (hPRL). The chloride concentration of sweat obtained a day later was significantly elevated. The concentration generally increased after a second and sometimes a third injection of anti-PRL. The average maximum sweat chloride obtained was 61.9 +/- 8.25 meq/liter. Serum of rabbits that had not been exposed to hPRL was prepared and diluted in the same way as the anti-hPRL. The chloride concentration of sweat of 3 mice that received the preparation for several days remained unchanged at the low normal level. We conclude that depletion of PRL increases the concentration of chloride in human sweat.

Animals↗

PubMed2003

Effect of skin temperature on the cholinergic sensitivity of the human eccrine sweat gland.

UNLABELLED: Although sweat gland activity is directly controlled by the central nervous system, which detects changes in core body temperature, sweat glands can also be influenced by local cutaneous thermal conditions. OBJECTIVE: The present study sought to determine the effect of local skin temperature on pilocarpine-induced sweating within a range of typical skin temperatures. METHODS: Thirteen subjects (30 +/- 6 years; 172 +/- 11 cm; 72.8 +/- 11.0 kg) had forearm sweat rates measured at rest following pilocarpine iontophoresis at each of three skin temperatures in randomized order: warm (T(warm) = 37.1 +/- 0.9 degrees C), control (T(con) = 32.3 +/- 1.4 degrees C), and cool (T(cool) = 26.6 +/- 1.3 degrees C). T(skin) was raised and lowered with an electric heating pad and gel ice pack, respectively. Forearm T(skin) was measured with a skin temperature probe. Pilocarpine iontophoresis was used on an approximately 7 cm(2) area of the anterior forearm to stimulate localized sweating. Following stimulation, sweat was collected from the area for 15 min with a Macroduct Sweat Collection System. RESULTS: There was a higher sweat rate at T(warm) (p = 0.001) and T(con) (p = 0.006) compared to that at T(cool). However, there was no difference between the sweat rate at T(warm) and that at T(con) (p = 0.127). CONCLUSION: These results indicated that skin temperatures below approximately 32 degrees C affect local sweat production primarily by altering glandular sensitivity to the neurotransmitter, whereas skin temperatures above approximately 32 degrees C predominantly affect neurotransmitter release. Furthermore, sweat glands display maximal or near maximal cholinergic sensitivity at resting skin temperature in a thermoneutral environment.

Acetylcholine↗

PubMed1990

Night sweats in Hodgkin's disease. A manifestation of preceding minor febrile pulses.

The authors verified the hypothesis regarding an unawareness of possible febrile alterations during night sleep in patients with Hodgkin's disease who complain of night sweats as their only symptom. In these patients, body temperature was monitored by means of a 0.01 degrees C-sensitive linear transducer coupled with a digital multimeter. The palm of the hand (after it was passively closed in a fist by a full bandage) was the body site where temperature measurement was found to be most comfortable for a sleeping patient and independent of movements during sleep. A good correlation was found between the hand temperature taken with this technique and oral temperature. Of six patients with sweating as their only symptom, sweating recurred during the night in four and during the afternoon in the other two. In all patients sweating was preceded by a critical 0.5 to 1.5 degrees C increase in hand temperature, which took place no more than 30 minutes before sweating. Those with nocturnal sweats awakened during the subsequent sweating-related, rapid temperature decrease. These results are consistent with the occurrence of slight unperceived febrile pulses that precede sweating. The only peculiarity of night sweats consists in the higher probability that a preceding slight temperature rise may not be perceived by a sleeping patient, who is more likely to be awakened by the discomfort of the subsequent sweating. This would also explain the small prognostic significance of these sweats, which is the same as that of the preceding fever. These results are discussed in light of the increasing clinical evidence that patients with Hodgkin's disease are often affected by an instability of the thermoregulatory hypothalamic centers.

Adolescent↗

PubMed1988

A comparative study of copper, lead, cadmium and zinc in human sweat and blood.

Zinc, cadmium, lead and copper in sweat from 24 male and 39 female volunteers were determined by anodic stripping voltammetry. Sweating was induced on the forearms by pilocarpine iontophoresis. Average values found for zinc, cadmium, lead and copper in sweat from males were 181 (range 25-863), 1.4 (less than 0.5-10), 41 (6-87) and 103 (less than 5-673) micrograms l-1, respectively. Zinc in sweat from females was significantly higher than in sweat from males (331 micrograms l-1, range 87-836 micrograms l-1), while sweat copper and sweat lead in females were lower (29 micrograms Cu l-1, range less than 5-146 micrograms Cu l-1 and 24 micrograms Pb l-1, range less than 5-66 micrograms Pb l-1). Those taking oral contraceptives showed increased sweat copper concentrations (94 micrograms Cu l-1, range less than 5-480 micrograms Cu l-1) and sweat lead concentrations (36 micrograms Pb l-1, range less than 5-70 micrograms Pb l-1). There was no sex-based difference for copper in sauna-induced sweat. Metal concentrations in sweat were compared with ceruloplasmin, alkaline phosphatase, and total and mobile copper and zinc concentrations in serum in males and females.

Cadmium↗

PubMed1982

Sweating in preterm babies.

The development of thermal sweating was investigated in 117 studies on 85 term and preterm infants. The babies were nursed naked in an incubator and exposed to progressively higher air temperatures until sweating occurred or until the rectal temperature reached 37.9 degrees C. Most babies of 36 weeks' gestation or more were able to sweat from the first day. Babies of less than 36 weeks' gestation did not sweat initially. However, postnatal existence hastened the development of sweating so that by 13 days all babies studied were able to sweat. Sweating occurred first and was most marked on the forehead. The intensity and extent of the sweat response depended on gestational age. With postnatal age the extent of the response rapidly increased but the intensity only rose slowly. The air temperature required to induce sweating was higher in the more immature babies but fell with postnatal ge. Although even the most immature infant soon develops the ability to sweat in response to heat stress, the efficiency of sweating as a thermoregulatory process is poor.

Gestational Age↗

PubMed1999

Monitoring cocaine use in substance-abuse-treatment patients by sweat and urine testing.

Sweat and urine specimens were collected from 44 methadone-maintenance patients to evaluate the use of sweat testing to monitor cocaine use. Paired sweat patches that were applied and removed weekly (on Tuesdays) were compared with 3-5 consecutive urine specimens collected Mondays, Wednesdays, and Fridays. All patches (N = 930) were extracted in 2.5 mL of solvent and analyzed by ELISA immunoassay (cutoff concentration 10 ng/mL); a subset of patches (N = 591) was also analyzed by gas chromatography-mass spectrometry (GC-MS) for cocaine, benzoylecgonine (BZE), and ecgonine methyl ester (EME) (cutoff concentration 5 ng/mL). Urine specimens were subjected to qualitative analysis by EMIT (cutoff 300 ng/mL) and subsets were analyzed by TDx (semiquantitative, LOD 30 ng/mL) and by GC-MS for cocaine (LOD 5 ng/mL). Results were evaluated to (1) determine the relative amounts of cocaine and its metabolites in sweat; (2) assess replicability in duplicate patches; (3) compare ELISA and GC-MS results for cocaine in sweat; and (4) compare the detection of cocaine use by sweat and urine testing. Cocaine was detected by GC-MS in 99% of ELISA-positive sweat patches; median concentrations of cocaine, BZE, and EME were 378, 78.7, and 74 ng/mL, respectively. Agreement in duplicate patches was approximately 90% by ELISA analysis. The sensitivity, specificity, and efficiency of sweat ELISA cocaine results as compared with sweat GC-MS results were 93.6%, 91.3%, and 93.2%, respectively. The sensitivity, specificity, and efficiency between ELISA sweat patch and EMIT urine results were 97.6%, 60.5%, and 77.7%, respectively. These results support the use of sweat patches for monitoring cocaine use, though further evaluation is needed.

Adolescent↗

PubMed2000

Variations in regional sweat composition in normal human males.

This project aimed to quantify the regional distribution of sweat composition over the skin surface and to determine whether sweat constituent concentrations collected from regional sites can estimate whole-body concentrations. Ten males cycled for 90 min in a 20 degrees C (50% relative humidity) environment at 45% peak aerobic power. Sweat was collected from eleven skin regions and the whole body, using a wash-down technique. Strong relationships were evident between the regional and whole-body sweat [Na+] and [Cl-], such that the thigh and calf exhibited greater correlation coefficients than area-weighted means derived from four and eight skin regions. Therefore, in this particular protocol the whole-body sweat [Na+] and [Cl-] could be predicted from regional sweat collections. Relationships between sweat constituents were evident for sweat [Na+] and pH, and sweat [K+] and [lactate] when data were pooled between skin regions and subjects. To our knowledge this is the first investigation to report a positive relationship between sweat [K+] and [lactate]. The exact mechanism responsible for the positive relationship between sweat [K+] and [lactate] is uncertain although it is speculated to occur at the secretory coil.

Adult↗

PubMed1982

Sweat composition in exercise and in heat.

Sweat samples were collected from the forearms of eight male volunteers using light gauze pads applied for 20-min periods. Preliminary trials indicated that this technique yielded realistic figures for both sweat volume and sweat composition. Tests were conducted under three conditions: a) outdoor exercise, cool environment; b) indoor exercise, normal room temperatures; and c) sauna exposure. In all environments, proximal forearm samples indicated a larger sweat secretion than distal forearm or hand samples. [Mg2+] decreased as sweat flow increased, but after allowance for interindividual differences of sweat volume, [Na+], [K+], [Ca2+], and [Cl-] were independent of sweat flow rates. The differential effect of sweat flow suggests active regulation rather than contamination. Interindividual differences of sweat composition could not be explained in terms of differences in personal fitness. Sauna bathing yielded sweat with a higher [Mg2+] and [Ca2+] content than did exercise; however, [Na+], [K+], and [Cl-] were similar for the three experimental conditions. Again, the data are best explained in terms of an active regulation of sweat composition. Total ionic losses do not seem sufficient to deplete body mineral reserves unless many days of training are undertaken in a hot climate.

Adult↗

PubMed2004

Mean body temperature does not modulate eccrine sweat rate during upright tilt.

Conflicting reports exist about the role of baroreflexes in efferent control of eccrine sweat rate. These conflicting reports may be due to differing mean body temperatures between studies. The purpose of this project was to test the hypothesis that mean body temperature modulates the effect of head-up tilt on sweat rate and skin sympathetic nerve activity (SSNA). To address this question, mean body temperature (0.9.internal temperature + 0.1.mean skin temperature), SSNA (microneurography of peroneal nerve, n = 8), and sweat rate (from an area innervated by the peroneal nerve and from two forearm sites, one perfused with neostigmine to augment sweating at lower mean body temperatures and the second with the vehicle, n = 12) were measured in 13 subjects during multiple 30 degrees head-up tilts during whole body heating. At the end of the heat stress, mean body temperature (36.8 +/- 0.1 to 38.0 +/- 0.1 degrees C) and sweat rate at all sites were significantly elevated. No significant correlations were observed between mean body temperature and the change in SSNA during head-up tilt (r = 0.07; P = 0.62), sweating within the innervated area (r = 0.06; P = 0.56), sweating at the neostigmine treated site (r = 0.04; P = 0.69), or sweating at the control site (r = 0.01; P = 0.94). Also, for each tilt throughout the heat stress, there were no significant differences in sweat rate (final tilt sweat rates were 0.69 +/- 0.11 and 0.68 +/- 0.11 mg.cm(-2).min(-1) within the innervated area; 1.04 +/- 0.16 and 1.06 +/- 0.16 mg.cm(-2).min(-1) at the neostigmine-treated site; and 0.85 +/- 0.15 and 0.85 +/- 0.15 mg.cm(-2).min(-1) at the control site, for supine and tilt, respectively). Hence, these data indicate that mean body temperature does not modulate eccrine sweat rate during baroreceptor unloading induced via 30 degrees head-up tilt.

Adult↗

PubMed2004

Painful sweating.

OBJECTIVE: The authors report a case of spontaneous and gustatory facial pain and sweating. METHODS: The patient had frequent episodes of pain, sweating, and flushing bilaterally in the hairless skin of the ophthalmic and maxillary distributions of the trigeminal nerve. Gustatory stimuli (e.g., orange juice, pickled onions) reliably evoked episodes, but episodes also frequently came on spontaneously. The problem had begun during adolescence, about the time of topical treatment and then electrocauteries for facial warts. The patient reported benefit from tricyclic antidepressants, guanethidine, and trospium chloride (an anti-cholinergic quaternary amine used in Europe for urinary urgency). There was no pain or excessive sweating in other body areas, nor pain with exercise. RESULTS: Administration of edrophonium IV evoked pain and sweating, and ganglion blockade by IV trimethaphan eliminated pain and sweating and markedly attenuated responses to edrophonium. Trospium chloride also prevented edrophonium-induced pain and sweating. Bicycle exercise produced the same increment in forehead humidity as in a spontaneous episode but did not evoke pain. Tyramine infusion did not bring on pain or sweating, whereas iontophoretic acetylcholine administration to one cheek evoked pain and sweating bilaterally. Topical glycopyrrolate cream eliminated spontaneous, gustatory, and edrophonium-induced episodes. CONCLUSIONS: The findings indicate that facial pain and sweating can result from occupation of muscarinic cholinergic receptors after acetylcholine release from local nerves. The authors propose that after destruction of cutaneous nerves, aberrant regenerant sprouting innervates sweat glands, producing gustatory sweating as in auriculotemporal syndrome (Frey syndrome), and innervates nociceptors, producing pain.

Acetylcholine↗

PubMed2005

Antidepressant-induced sweating.

OBJECTIVE: To report a case of excessive sweating probably caused by paroxetine, review the literature on antidepressant-induced sweating, and provide recommendations for the management of antidepressant-induced sweating. CASE SUMMARY: A 59-year-old white female presented to a pharmacist-staffed pharmacotherapy clinic with episodes of excessive sweating. The episodes occurred primarily on her head and back of the neck. Other etiologies were ruled out and paroxetine was discontinued. Paroxetine had been initiated at least 7 months prior to the reporting of symptoms. Sweating symptoms gradually improved until resolution 5 weeks following discontinuation of paroxetine. The Naranjo probability scale indicated a causal relationship is probable. DISCUSSION: Excessive sweating has been associated with antidepressants including tricyclic antidepressants, selective serotonin-reuptake inhibitors, and venlafaxine. In some patients, these symptoms require therapeutic intervention such as dose reduction, antidepressant substitution, antidepressant discontinuation, or addition of an agent to control sweating. Agents that have been reported successful in controlling the sweating include benztropine and cyproheptadine. CONCLUSIONS: We recommend a patient-specific approach for the management of antidepressant-induced sweating. First, consider dose reduction or a trial off antidepressant medication. In patients in whom this is inappropriate or ineffective, substitution of another antidepressant should be considered. If episodes of excessive sweating persist, consider treatment of sweating symptoms with benztropine or cyproheptadine in the absence of contraindications.

Antidepressive Agents↗

PubMed1999

Comparison of three methods for estimation of exercise-related ion losses in sweat of horses.

OBJECTIVE: To quantify total fluid loss in sweat of Thoroughbreds during >3 hours of low-intensity exercise in controlled conditions and to calculate and compare estimated ion losses in sweat, according to 3 methods. ANIMALS: 6 exercise-trained Thoroughbreds. PROCEDURE: Fluid and ion losses in sweat were measured in 6 horses exercising at 40% of the speed that elicited maximum oxygen consumption for 45 km. Horses were given a 15-minute rest period at the end of three 15-km exercise phases. Horses completed 2 exercise trials. Ion losses in sweat were calculated, using measurements of local sweating rate and sweat ion composition (SWT), change in net exchangeable cation content (CAT), and change in extracellular ion content (PLAS) derived from plasma total solids and ion concentrations. RESULTS: Measurement of SWT revealed a mean (+/- SEM) fluid loss in sweat during 45 km of exercise of 27.5 +/- 1.6 L. Total ion loss in sweat was approximately 241 g or 7.8 mol with higher sodium losses in the second and third phases of exercise compared with the first phase. Losses of sodium and potassium calculated by SWT or CAT were not significantly different from each other, whereas losses of these ions as determined by PLAS were significantly lower. CONCLUSIONS AND CLINICAL RELEVANCE: Calculation of ion losses from a mean whole body sweating rate extrapolated from either local sweating rate and sweat ion composition or from change in net exchangeable cation content provide similar results, whereas ion losses determined by changes in extracellular ion content derived from plasma total solids and ion concentration results in underestimation of actual losses.

Animals↗

PubMed2002

[Study on the relationship between epidermal stem cells and the developing process of sweat gland in human fetal skin].

OBJECTIVE: To explore the relationship between epidermal stem cells and the developing process of sweat gland in human fetal skin, so as to obtain a hint for future induction of epidermal stem cells to differentiate into sweat gland cells. METHODS: Total layer of human skin from the back of fetus at gestational ages from 11 to 31 weeks, obtained from spontaneous abortion was routinely examined. The expressions of beta1 integrin and keratin 19 in sweat gland cords or buds and mature sweat gland cells were dynamically observed with SP immunohistochemical technique. The development and maturation of sweat gland were identified by the positive staining of keratin 8 with immunohistochemistry. RESULTS: It was revealed by histologic observation that basal layer cells of the primary epidermal ridge exhibited focal aggregation and formed hillocks at 16 gestational weeks. The hillocks of cells then migrated downward as cords into the dermis during 18 - 20 gestational weeks. Then, the end part of the cell cord developed into a round lump of twining cords assuming the mature sweat gland. The expressions of beta1 integrin and keratin 19 were found not only in sweat gland cords and buds but also in the mature cells and lasted throughout the total period of sweat gland development. The expression of keratin 8 in sweat gland buds started since 14 - 16 gestational weeks and maintained thereafter. CONCLUSION: The sweat gland started to develop during 14 - 16 gestational weeks and matured at 24 weeks. During the development process of sweat gland, epidermal stem cells were considered to be the key source.

Aborted Fetus↗

PubMed2002

Uric acid and urea in human sweat.

The present study investigated whether thermal sweating may relieve elevated concentrations of serum uric acid or urea. Concentrations of uric acid and urea were measured in the sweat of sixteen male volunteers, who were treated with external heat after one hour of intense physical exercise. The same analytes were also measured in their urine and serum samples. Furthermore, creatinine and some electrolytes were determined in these specimens. The results show that the concentration of uric acid in the sweat is 24.5 micromol/L, which is only 6.3% of that in serum. The concentration of urea in the sweat is 22.2 mmol/L, which is 3.6 times that in serum. The results indicate that sweat uric acid concentration is quite minimal, and the estimated total uric acid excretion per day in normal physiological range is insignificant. However, the level of sweat urea was found at a much higher concentration than the serum level. No correlation could be established between the level of uric acid in sweat and in serum. There was also no correlation between the level of urea in sweat and that in serum. These results suggest it would not be effective to relieve the elevated serum uric acid concentration by thermal sweating when the renal excretion of uric acid is partly compromised. Nevertheless, the potential of urea excretion via profuse sweating is apparent particularly when the kidneys are damaged or their function is impaired. These findings also suggest that persons who take vigorous exercise or are exposed to hot environments should be well advised to drink adequate fluids since heavy sweating excretes only minimal uric acid, accompanied by significant diminution of urinary output and diminished urinary excretions of uric acid, which may induce elevated levels of serum uric acid.

Adult↗

PubMed1984

Quantitation of the sweating deficiency in diabetes mellitus.

This report introduces quantitative tests for the evaluation of sweating and the results obtained in 81 diabetic and 30 control subjects. The tests rely on the ability of pilocarpine, introduced into the skin by iontophoresis, to stimulate sweating from fully or partially innervated sweat glands but not from denervated glands. Many diabetic patients had a reduced number of excitable sweat glands and a low volume of sweat per square centimeter of skin. The results of the sweat tests correlated best with the clinically determined perception of pain from pinprick. The similar degree of involvement of sudomotor axons and pain-conveying axons may be related to the known similarity in size and reinnervation patterns. There was poor correlation of the sweating deficiency with alpha motor conduction velocity and with denervation of foot muscles as determined by the evoked muscle action potential. The number of excitable sweat glands was usually normal if the muscle action potential was above 0.5 mv, and often normal even when a muscle action potential was unobtainable. Every diabetic patient with abnormal sweating and several with normal sweating had reduced heart rate fluctuation during a standard Valsalva maneuver or during slow respiration.

Adult↗

PubMed2000

Gender differences in sweat lactate.

Sweat rate may affect sweat lactate concentration. The current study examined potential gender differences in sweat lactate concentrations because of varying sweat rates. Males (n = 6) and females (n = 6) of similar age, percentage body fat, and maximal oxygen consumption (VO2max) completed constant load (CON) cycling (30 min--approximately 40% VO2max) and interval cycling (INT) (15 1-min intervals each separated by 1 min of rest) trials at 32 (1) degrees C wet bulb globe temperature (WBGT). Trials were preceded by 15 min of warm-up (0.5 kp, 60 rpms) and followed by 15 min of rest. Blood and sweat samples were collected at 15, 25, 35, 45, and 60 min during each trial. Total body water loss was used to calculate sweat rate. Blood lactate concentrations (CON approximately equal to 2 mmol.l-1, INT approximately equal to 6 mmol.l-1) and sweat lactate concentrations (CON and INT approximately equal to 12 mmol.l-1) were not significantly different (P > 0.05) at any time between genders for CON or INT. Overall sweat rates (ml.h-1) were not significantly different (P > 0.05) between trials but were significantly greater (P < or = 0.05) for males than for females for CON [779.7 (292.6) versus 450.3 (84.6) ml.h-1] and INT [798.0 (268.3) versus 503.0 (41.4) ml.h-1]. However, correcting for surface area diminished the difference [CON: 390.7 (134.4) versus 277.7 (44.4) ml.h-1, INT: 401.5 (124.1) versus 310.6 (23.4) ml.h-1 (P < or = 0.07)]. Estimated total lactate secretion was significantly greater (P < or = 0.05) in males for CON and INT. Results suggest that sweat rate differences do not affect sweat lactate concentrations between genders.

Adult↗

PubMed1999

Gustatory sweating: clinical implications and etiologic aspects.

PURPOSE: It was the aim of this study to provide detailed general information on the clinical picture of different kinds of gustatory sweating, including reevaluation of a series of patients who underwent parotidectomy, removal of the submandibular gland, or neck dissection. PATIENTS AND METHODS: This study summarizes the statements of 548 patients questioned about the occurrence of gustatory sweating after parotidectomy (n = 296), extirpation of the submandibular gland (n = 79), and neck dissection (n = 173). RESULTS: After parotidectomy, 45% of the patients had noticed gustatory sweating. In most of them (70%), the symptoms began within 6 months after surgery. Gustatory sweating developed in only one patient with submandibular extirpation (1.5%), and not at all after neck dissection. Most patients (52%) reported that the symptoms occurred independent of the kind of food ingested. These results show that the "masticatory component" is an important trigger for Frey's syndrome. Application of Minor's test localized gustatory sweating mainly in the region of previous parotid lobe removal, but also in other areas deriving their sensory supply from the auriculotemporal, greater auricular, and lesser occipital nerves. The size of the area affected by the sweating was similar after lateral and total parotidectomy. When evaluating clinical symptoms, subjective assessment by the patients seemed to play a major role. After submandibular extirpation and neck dissection, some patients reported gustatory sweating that was not verified by Minor's test. CONCLUSION: There is general agreement that the cause of gustatory sweating is sympathetic or parasympathetic innervation of previously denervated sweat glands, initiated by gustatory triggers. The location of the "erroneous innervation" depends on the type of lesion. In cases after parotidectomy, misdirected parasympathetic regeneration is the model integrating all known factors into a rational concept. For didactic and systematic-pragmatic reasons, a clinically oriented classification of gustatory sweating (types I to III) seems to be useful.

Chi-Square Distribution↗

PubMed1966

Composition of the secretion from the eccrine sweat glands of the cat's foot pad.

1. The sweat composition from the cat's foot pad was examined at various rates of secretion. Sodium pentobarbitone or chloralose anaesthesia were used.2. Cat's pad sweat contains lactate, glucose is almost absent, and the sodium and chloride concentrations increased with increasing sweat rate. In these respects the secretion resembles human eccrine sweat.3. The sodium, chloride, and potassium concentrations are much higher than in human sweat; also the potassium level decreased with increasing rate. Consequently, whereas human sweat is hypotonic with respect to the plasma, cat's pad sweat is slightly hypertonic with respect to the plasma even at low rates of secretion. In contrast to human sweat glands, which produce a slightly acidic secretion containing ammonia, cat's pad sweat glands produce an alkaline secretion containing bicarbonate. Also in contrast to human sweat, lactate levels decreased with increasing sweat rate.

Animals↗