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PubMed2000

Excretion of beta-lactam antibiotics in sweat--a neglected mechanism for development of antibiotic resistance?

The concentrations of beta-lactam antibiotics after standard doses were measured in blood and apocrine (axilla) and eccrine (forearm) sweat from six adult healthy persons. All persons had ceftazidime (axilla, 28.4 microg/ml; forearm, 11 microg/ml) and ceftriaxone (axilla, 8.9 microg/ml; forearm, 2.5 microg/ml) in sweat, and one person had cefuroxime in sweat (axilla, 7.8 microg/ml) (all data are mean peaks). Three persons had benzylpenicillin (axilla, 2.6 to 0.1 microg/ml) and one had phenoxymethylpenicillin (axilla, 0.4 microg/ml) in sweat. Excretion of beta-lactam antibiotics in the sweat may explain why staphylococci so rapidly become resistant to these drugs.

Administration, Oral↗

PubMed2004

Sweat testing in newborns positive to neonatal screening for cystic fibrosis.

Sweat chloride concentrations above 40 mmol/l are unusual in newborns screened for cystic fibrosis and should be followed up. Centiles of sweat chloride concentrations in newborns positive to cystic fibrosis neonatal screening are presented. There are no significant correlations between age at sweat testing and sweat chloride concentration or quantity of sweat collected.

Aging↗

PubMed1989

Fractional measurements of sweat osmolality in patients with cystic fibrosis.

After pilocarpine iontophoresis the change of sweat concentration during collection was studied by vapour pressure osmometry in 24 patients with cystic fibrosis and 24 healthy controls. There was a continuous but proportionate fall in sweat concentrations during the collection period. Mean (SD) initial sweat concentration in the control group was 154.4 (32.6) mmol/kg falling, after 50 microliters of sweat produced, to 92.9 (15.8) mmol/kg. In the cystic fibrosis group it was 315.9 (35.8) mmol/kg falling to 247.4 (24.9) mmol/kg. Despite different rates of fall in concentrations, separation of the two groups was maintained throughout. We conclude that there are implications for the potential improvement of the predictive value of the sweat test.

Adolescent↗

PubMed2005

Sweat rate and fluid turnover in American football players compared with runners in a hot and humid environment.

OBJECTIVES: To determine sweat rate (SwR) and fluid requirements for American footballers practicing in a hot, humid environment compared with cross country runners in the same conditions. METHODS: Fifteen subjects, 10 footballers and five runners, participated. On the 4th and 8th day of preseason two a day practices, SwR during exercise was determined in both morning and afternoon practices/runs from the change in body mass adjusted for fluids consumed and urine produced. Unpaired t tests were used to determine differences between groups. RESULTS: Overall SwR measured in litres/h was higher in the footballers than the cross country runners (2.14 (0.53) v 1.77 (0.4); p<0.01). Total sweat loss in both morning (4.83 (1.2) v 1.56 (0.39) litres) and afternoon (4.8 (1.2) v 1.97 (0.28) litres) practices/runs, and daily sweat losses (9.4 (2.2) v 3.53 (0.54) litres) were higher in the footballers (p<0.0001). The footballers consumed larger volumes of fluid during both morning and afternoon practices/runs (23.9 (8.9) v 5.5 (3.1) ml/min and 23.5 (7.3) v 13.6 (5.6) ml/min; p<0.01). For complete hydration, the necessary daily fluid consumption calculated as 130% of daily sweat loss in the footballers was 12.2 (2.9) litres compared with 4.6 (0.7) litres in the runners (p<0.0001). Calculated 24 hour fluid requirements in the footballers ranged from 8.8 to 19 litres. CONCLUSIONS: The American footballers had a high SwR with large total daily sweat losses. Consuming large volumes of hypotonic fluid may promote sodium dilution. Recommendations for fluid and electrolyte replacement must be carefully considered and monitored in footballers to promote safe hydration and avoid hyponatraemia.

Adult↗

PubMed1983

Sweat tests to diagnose cystic fibrosis in adults.

Twenty five patients with cystic fibrosis and 25 controls were studied to define a sweat sodium concentration in adults that could be taken as diagnostic of cystic fibrosis. Some of the controls had a sweat sodium concentration of over 50 mmol(mEq)/l, and thus cystic fibrosis should be diagnosed in an adult only when two measurements of sweat sodium concentration are above 70 mmol/l. In cases in which the sweat sodium concentration was borderline a suppression test using fludrocortisone improved the accuracy of diagnosis; this test entails recording the lowest concentration reached after administration of the drug. A scatter diagram of the baseline sweat sodium concentrations plotted against the lowest concentration attained after suppression with fludrocortisone may aid the diagnosis further.

Adolescent↗

PubMed1992

Detection of subclinical autonomic neuropathy in constipated patients using a sweat test.

Chronic idiopathic constipation may be the result of an autonomic neuropathy. This hypothesis was tested in 23 constipated patients and 17 age matched controls, using the acetylcholine sweat spot test devised to test autonomic integrity in diabetes. Acetylcholine (0.01%) was injected in the dorsum of the foot painted with a mixture of starch and iodine. Active sweat glands appeared on the surface of the skin as small black dots which were photographed and counted, using a grid with 60 subareas. Two measurements were made: the number of dots per unit subarea (sweat spot test score) and the % number of abnormal subareas (with less than six spots). These two parameters were correlated. The median sweat spot test score was 9.53 in patients and 13.92 in controls (p = 0.0001), the receiver operating characteristic curve showing that a score of 12 delimited normal and abnormal subjects. Increasing age was correlated with a low score in patients, probably because of prolonged symptoms. Seventy per cent of patients and one control had a borderline or abnormal number of subareas. These results suggest that idiopathic constipation is associated with a degree of autonomic denervation. The sweat spot test is an easy, inexpensive method to test this hypothesis and deserves a place in the clinical assessment of slow transit constipated patients.

Acetylcholine↗

PubMed1988

Harlequin syndrome: the sudden onset of unilateral flushing and sweating.

Facial flushing and sweating were investigated in five patients who complained of the sudden onset of unilateral facial flushing in hot weather or when exercising vigorously. One patient probably suffered a brainstem infarct at the time that the unilateral flush was first noticed, and was left with a subtle Horner's syndrome on the side opposite to the flush. The other four had no other neurological symptoms and no ocular signs of Horner's syndrome. Thermal and emotional flushing and sweating were found to be impaired on the non-flushing side of the forehead in all five patients whereas gustatory sweating and flushing were increased on that side in four of the five patients, a combination of signs indicating a deficit of the second sympathetic neuron at the level of the third thoracic segment. CT and MRI of this area failed to disclose a structural lesion but latency from stimulation of the motor cortex and thoracic spinal cord to the third intercostal muscle was delayed on the non-flushing side in one patient. The complaint of unilateral flushing and sweating was abolished in one patient by ipsilateral stellate ganglionectomy. The unilateral facial flushing and sweating induced by heat in all five patients was thus a normal or excessive response by an intact sympathetic pathway, the other side failing to respond because of a sympathetic deficit. The onset in the four cases of peripheral origin followed strenuous exertion, which suggested that an anterior radicular artery may have become occluded at the third thoracic segment during torsion of the thoracic spine.

Adult↗

PubMed1989

Core threshold temperatures for sweating.

To detect shifts in the threshold core temperature (Tc) for sweating caused by particular nonthermal stresses, it is necessary to stabilize or standardize all other environmental and physiological variables which cause such shifts. It is, however, difficult to cause progressive changes in Tc without also causing changes in skin temperature (Tsk). This study compares the technique of body warming by immersion in water at 40 degrees C, and subsequent body cooling in water at 28 degrees C, to determine the core threshold for sweating, with one by which Tc was raised by cycling exercise in air at 20 degrees C, and then lowered by immersion in water at 28 degrees C. The first of these procedures involved considerable shifts in Tsk upon immersion in water at 40 degrees C, and again upon transfer to water at 28 degrees C; the second procedure caused only small changes in Tsk. The onset of sweating at a lower esophageal temperature (Tes) during immersion in water at 40 degrees C (36.9 +/- 0.1 degrees C) than during exercise (37.4 +/- 0.3 degree C) is attributed to the high Tsk since Tes was then unchanged. Likewise, the rapid decline in the sweat rate during immersion at 28 degrees C had the same time course to extinction after the pretreatments. This related more to the Tsk, which was common, than to the levels or rates of change of Tes, which both differed between techniques. Tes fell most rapidly, and thus sweating was extinguished at a lower Tes, following 40 degrees C immersion than following exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Air↗

PubMed1979

Mechanical properties and functions of the myoepithelium in the eccrine sweat gland.

Contractile properties of an isolated segment of the secretory coil of the monkey palm eccrine sweat gland were studied in vitro with a transducer. Contraction of up to 10 mgf was induced with acetylcholine but not with alpha or beta adrenergic agonists, caffeine, prostaglandin E1, or by a calcium ionophore A23187. Other features included K+ contracture, staircase effect, poor extensibility, length-tension relationship with a peak tensile response at 115--120% of the resting length, and requirement of Ca2+. The function of myoepithelium is unlikely to expulse the preformed sweat because the amount of preformed sweat is small, K+-contracture failed to expulse sweat, and because myoepithelial contraction was not induced by such stimulants of sweat secretion as A23187, phenylephrine, isoproterenol, and prostaglandin E1. The maximal transverse tension of 20 mgf during acetylcholine stimulation under resting tension was calculated to support the luminal hydrostatic pressure of approximately 500 mmHg. Thus the function of the myoepithelium may be to render structural support for the secretory epithelium.

Acetylcholine↗

PubMed1975

Circadian variations in the sweating mechanism.

Sweat rates and body temperatures of human subjects were measured at 0200, 1000, and 1800 h during a heat exposure of 90 min. The latent period of sweating was not significantly altered in the evening but significantly shortened during the night. Mean body temperature corresponding to the onset of sweating was nearer to the basal body temperature during the night, while during the day the difference between these two temperatures became larger. This phenomenon seems related to the circadian cycle of vasomotor adjustment, since during the night body conductance was higher than during the day and corresponded to a state of a vasodilatation similar to that observed at the onset of sweating. During the day, this situation was reversed. During steady state, the following changes were observed: sweating rate, night less than morning less than evening; skin temperatures, night less than morning less than evening; and rectal temperature increase, morning less than evening less than night. It is hypothesized that these changes are due to either different metabolic rates or an imbalance between heat gains and losses which preserve the circadian rhythm of the body temperature, even under thermal loads.

Body Temperature Regulation↗

PubMed1976

Acclimatization in a hot, humid environment: energy exchange, body temperature, and sweating.

Four trained young men, worked for 4 h/day at 43-50% of their maximum aerobic capacity for 3 days at 25 degrees C db, 18 degrees C wb and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. Their thermal status was assessed using direct calorimetry. As a group, the men showed classical acclimization responses, but there were marked individual differences. The calorimetric analysis revealed that reductions in strain were associated with minor changes in heat balance confined to the first and last hours of exposure. Events occurring within the first 4 days appeared to have little effect on body temperatures. Significant decreases in body temperature took place only when sweat and evaporation rate increased. A 10% increase in evaporation rate was accompanied by a 30% increase in sweat rate and a 200% increase in unevaporated sweat; thus, there is a wasteful overproduction of sweat. By the 10th day skin temperature was confined to the level necessary to evaporate sufficient sweat to achieve thermal balance with a fully wet body surface. The efficiency of heat transport within the body did not change with acclimatization.

Acclimatization↗

PubMed1979

Role of skin temperature in the control of sweating.

In five male subjects tympanic membrane temperature (Tty), rectal temperature, skin temperatures at 12 sites were simultaneously recorded. Local sweating rate was measured at six sites using resistance hygrometry. After steady-state sweating was established, the lower body was heated at ambient temperatures of 50, 60, 70, and 80 degrees C or cooled at an ambient temperature of 29 degrees C while the upper body remained at a constant ambient temperature. During lower body heating or cooling, Tty was maintained constant by the drinking of cold (10 degrees C) or warm (45 degrees C) water. Sweating rate on both upper and lower body surfaces was proportional to lower body skin temperature. The regression coefficients for sweating rate versus mean lower body skin temperature varied from 0.03 to 0.09 mg/cm2.min. degrees C between subjects, but were not significantly different from each other (P greater than 0.05). This study demonstrates an influence of cutaneous thermoreceptors on sweating rate under steady-state conditions.

Humans↗

PubMed1981

Effect of blood volume on sweating rate and body fluids in exercising humans.

Five relatively fit men performed cycle ergometer exercise (65-70% VO2max) for up to 30 min at 30 degrees C, 40% rh. The data from control (normo-volemic), hypovolemic [8.7% reduction in blood volume (BV) induced by diuretics], and hypervolemic [7.9% expansion of BV induced by infusion if isotonic serum albumin] tests revealed significant effects of BV on body fluid and sweating responses. During control exercise, BV decreased an average (+/- SE) 370 +/- 64 ml at 20 min. A significantly smaller loss occurred after 20 min of hypovolemic exercise (270 +/- 29 ml). The decrease in BV during 30 min of hypervolemic exercise (541 +/- 43 ml) was significantly greater than during control (421 +/- 50 ml). Blood volume reduction also significantly altered the control of sweating rate independent of changes in plasma osmolality. The slope of the sweating rate-to-esophageal temperature relationship (SR/Tes) was significantly reduced from the mean value of 1.07 +/- 0.16 and 1.09 +/- 0.18 mg X min-1 X cm-2 X degrees C-1 during control tests, measured from the chest and arm, respectively, to 0.64 +/- 0.11 and 0.63 +/- 0.11 mg X min-1 X cm-2 X degrees C-1 during hypovolemia. The SR/Tes slope was unchanged in hypovolemia over active tissues (calf). Hypervolemia had no effect on the control of sweating at any site. Both the body fluid and sweating responses during hypovolemia act to conserve circulating blood volume during exercise.

Adult↗

PubMed1986

Plasma aldosterone and sweat sodium concentrations after exercise and heat acclimation.

This investigation was designed to determine the relationship between the levels of plasma aldosterone and eccrine sweat gland sodium excretion following exercise and heat acclimation. Ten subjects exercised at 45% of their maximal O2 uptake in a hot (40 degrees C), moderately humid (45% relative humidity) environment for 2 h/day on ten consecutive days. Acclimation was verified by significant reductions in exercise heart rate, rectal temperature, and heat storage, as well as significant elevation of resting plasma volume (12%, P less than 0.05) and exercise sweat rate on day 10 compared with day 1 of acclimation. During exercise, the concentration and total content of sodium in sweat as well as plasma aldosterone were significantly decreased from day 1 to day 10. The ratio of sweat sodium reabsorbed to plasma aldosterone concentration was significantly increased from day 1 to day 10 after both 1 and 2 h of exercise. These data indicate that plasma aldosterone concentrations decrease following heat acclimation; and eccrine gland responsiveness to aldosterone, as represented by sweat sodium reabsorption, may be augumented through exercise and heat acclimation.

Acclimatization↗

PubMed1987

Thiol-dependent aminopeptidase (350,000 mol wt) as a marker of epidermal contamination in sweat.

L-Leucine 2-naphthylamide (Leu-NA) hydrolytic activity is increased 20-fold in eccrine sweat collected by simple scraping (SS) compared with sweat collected over the white petrolatum (Vaseline) barrier (clean sweat, CS) [Am. J. Physiol. 250 (Regulatory Integrative Comp. Physiol. 19): R691-R698, 1986]. Sephadex G-200 chromatography of SS but not that of CS showed a single peak of Leu-NA hydrolytic activity (at pH 8) at 350,000 mol wt. An enzyme with similar molecular weight was eluted from tape-stripped stratum corneum and from stripped skin in situ. Anion-exchange FPLC of the 350,000 fractions yielded a single Leu-NA hydrolase peak at pH 8 (pool IV), which also showed hydrolytic activity for benzoyl-L-arginine-2-naphthylamide (BANA). Both Leu-NA and BANA hydrolytic activities of pool IV were thiol dependent, inhibited by heavy metals, and activated by ethylenediaminetetraacetic acid. The pool IV enzyme also hydrolyzed L-lysine- and L-arginine-2-naphthylamide. The most prominent BANA hydrolase activity was seen in both SS and CS at pH 5.0 at 33,000, which was not associated with Leu-NA hydrolytic activity. Diethylaminoethyl cellulose chromatography of the 33,000 fractions yielded three peaks of BANA hydrolytic activity in SS but only one in CS, suggesting that this thiol-dependent BANA hydrolyzing enzyme in CS may be of sweat gland origin. We conclude that the 350,000 thiol-dependent Leu-NA-hydrolyzing aminopeptidase is one of the most prominent epidermal contaminants and thus is a useful marker of epidermal contamination in sweat samples.

Adult↗

PubMed1989

Effect of cerebrospinal fluid hyperosmolality on sweating in the heat-stressed patas monkey.

Dehydration increases the osmolality of body fluids and decreases the rate of sweating during thermal stress. By localizing osmotic stimuli to central nervous system tissues, this study assessed the role of central stimulation on sweating in a heat-stressed nonhuman primate. Lenperone-tranquilized patas monkeys (Erythrocebus patas n = 5), exposed to 41 +/- 2 degrees C, were monitored for calf sweat rate, rectal and mean skin temperatures, oxygen consumption, and heart rate during infusions (255-413 microliters) of hypertonic artificial cerebrospinal fluid (ACSF) into the third cerebral ventricle. ACSF made hypertonic with NaCl to yield osmolalities of 800 and 1,000 mosmol/kgH2O significantly decreased sweat rate compared with control ACSF (285 mosmol/kgH2O), achieving maximal reductions during infusion of 37 and 53%, respectively. Rectal temperature significantly increased during the recovery period, reaching elevations of 0.69 and 0.72 degrees C, respectively, at 20 min postinfusion. In contrast, ACSF made hypertonic with sucrose (800 mosmol/kgH2O) failed to change sweat rate or rectal temperature during infusion in three animals. Thus, intracerebroventricular infusions of hypertonic ACSF mimicked dehydration-induced effects on thermoregulation. The reduction in heat loss during infusion appeared to depend on an elevation in cerebrospinal fluid [Na+] and not osmolality per se.

Animals↗

PubMed1992

Effects of varied air velocity on sweating and evaporative rates during exercise.

This study was designed to determine the extent to which changes in the evaporative power of the environment (Emax) affect sweating and evaporative rates. Six male subjects undertook four 60-min bouts of cycle ergometer exercise at 56% maximal O2 uptake (VO2max).Emax was varied by differences in ambient temperature and airflow; two exercise bouts took place at 24 degrees C and two at 35 degrees C, with air velocity at < 0.2 and 3.0 m/s in both. Total sweat production was estimated from body weight loss, whereas whole body evaporative rate was measured continuously from a Potter beam balance. Body core temperature was measured continuously from a thermocouple in the esophagus (T(es)), with mean skin temperature (Tsk) computed each minute from thermocouples at eight sites. Total body sweat loss was significantly greater (P < 0.05) in the 0.2- than in the 3.0-m/s condition at both 24 and 35 degrees C. Tsk was higher (P < 0.05) in the still-air conditions at both temperatures, but final T(es) was significantly higher (P < 0.05) in still air only in the 35 degrees C environment. Thus the reduced Emax in still air caused a greater heat storage, thereby stimulating a greater total sweat loss. However, in part because of reduced skin wettedness, the slope of the sweat rate-to-T(es) relation at 35 degrees C in the 3.0-m/s condition was 118% that at 0.2 m/s (P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Reproducibility of core temperature threshold for sweating onset in humans.

The control of sweating in humans has been described quantitatively in terms of skin and core temperatures (Tsk and Tcore, respectively). However, the precision with which features of the relationship between sweat rate and Tcore at a given Tsk can be reproduced in the short term is not known. We focused on the threshold Tcore. We held Tsk at 38 degrees C until sweating began for two periods separated by a period of cooling with Tsk at 32 degrees C in six men and three women. The esophageal temperature (Tes) at which sweating began was invariably lower in the second period of heating (average difference 0.09 degree C; maximum 0.17 degree C). Also, the rate of rise in Tes was invariably higher (average 148%) during the second period of heating. Thus, although a threshold cannot be reproduced within the error of Tes measurement, the consistency and small magnitude of the downward shift recommend our protocol as a practical method for evaluating other influences on thermoregulation, provided that the effects are big enough to be seen against a background of an expected small decrease. From the fundamental point of view, the consistency of the downward displacement has provocative implications, e.g., the rate of change in Tcore influences sweating or thermosensitive units in slow-responding thermal compartments contribute to the Tcore input signal.

Adult↗