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PubMed1984

Effect of hyperosmolality on control of blood flow and sweating.

To study the effect of hyperosmolality on thermoregulatory responses, five men [average maximal O2 consumption (VO2 max) = 48 ml X kg-1 X min-1] cycled at 65-75% VO2max for up to 30 min in a 30 degrees C, 40% relative humidity environment under three conditions. First, control tests (C) were performed where preexercise plasma volume (PV) and osmolality (Osm) averaged 3,800 ml and 282 mosmol X kg-1, respectively. Second, exercise tests (D) were performed following dehydration induced by fluid restriction and mild exercise (30% VO2max) in hot (40 degrees C) ambient conditions. Each subject then rested in cool surroundings 1 h before performing the exercise test. Preexercise PV and Osm averaged 3,606 ml and 293 mosmol X kg-1, respectively. Third, exercise tests (I) were performed following dehydration, but during the 1-h rest interval, 3% saline was infused so that PV was restored to 3,826 ml and Osm averaged 294 mosmol X kg-1 prior to exercise. During D, esophageal temperatures (Tes) were significantly higher than C, an avg 0.56 degrees C after 20 min exercise due to a 0.22 degrees C increase in Tes threshold for vasodilation, a 39% reduction in slope of the forearm blood flow (BF)-Tes relationship, a 32% average reduction in maximal exercise BF, and a 0.22 degrees C increase in Tes sweating threshold. During I, responses were similar to D, except the BF-Tes slope and the maximum BF were not significantly different from C. Thus hyperosmolality modifies thermoregulation by elevating thresholds for both vasodilation and sweating even without decreases in PV.

Adult↗
PubMed1985

Sweat rate vs. forearm blood flow during lower body negative pressure.

Skin blood flow is inhibited when hyperthermia and added hypovolemic stresses are superimposed. We tested the hypothesis that part of this inhibition is a reduced drive for cutaneous active vasodilatation (AVD) with sweat rate (SR) taken as an indirect measure of the efferent drive for cutaneous AVD. We also inquired whether SR itself changes with redistribution of blood volume. Six healthy supine men were subjected to lower body negative pressure (LBNP) after heating in water-perfused suits increased esophageal temperatures (Tes) to a mean of 37.2 degrees C and at least doubled SR and forearm vascular conductance (FVC). Heating continued throughout LBNP and recovery. Sweat rate did not decrease with LBNP onset, although SR-Tes slopes during LBNP were reduced 28% from control. In four subjects the SR-Tes slope did not recover when LBNP was discontinued. These observations suggest that SR is not an effector of the low-pressure baroreflex. In contrast to SR, FVC abruptly fell 22% at the onset of LBNP. Thereafter, FVC-Tes slopes near zero or less occurred. The major effector for FVC inhibition with LBNP appears to be the neural vasoconstrictor system. A minor component due to reduced drive for cutaneous AVD probably occurs as well.

Adult↗
PubMed1985

Influence of menstrual cycle on shivering, skin blood flow, and sweating responses measured at night.

In 10 women, external cold and heat exposures were performed both in the middle of luteal phase (L) and in the early follicular phase (F) of the menstrual cycle. Serum progesterone concentrations in L and F averaged 46.0 and 0.9 nmol X l-1, respectively. The experiments took place between 3:00 and 4:30 A.M., when the L-F core temperature difference is maximal. At neutral ambient temperature, esophageal (Tes), tympanic (Tty), rectal (Tre), and mean skin (Tsk) temperatures averaged 0.59 degrees C higher in L than in F. The thresholds for shivering, chest sweating, and cutaneous vasodilation (heat clearance technique) at the thumb and forearm were increased in L by an average of 0.47 degrees C, related to mean body temperature [Tb(es) = 0.87Tes + 0.13 Tsk] and to Tes, Tty, Tre, or Tsk. The above-threshold chest sweat rate and cutaneous heat clearances at the thumb and forearm were also enhanced in L, when related to Tb(es) or time. The metabolic rate, arm blood flow, and heart rate at thermoneutral conditions were increased in L by 5.0%, 1.1 ml X 100 ml-1 X min-1, and 4.6 beats X min-1, respectively. The concomitant increase in threshold temperatures for all autonomic thermoregulatory responses in L supports the concept of a resetting of the set point underlying the basal body temperature elevation in L. The effects of the increased threshold temperatures are counteracted by enhanced heat loss responses.

Analysis of Variance↗
PubMed1987

Sweating, hemodynamic responses, and thermal equilibration during hyperthermia in humans.

Hyperthermia, to 42 degrees C, for treatment of cancer, was induced 23 times in 13 anesthetized patients utilizing an extracorporeal heat-exchange circuit. Sweating rate over the chest, abdomen, arm and forearm ranged from 0.2 to 0.9 mg sweat X min-1 X cm-2. Cardiac index (CI), stroke volume index (SVI), left ventricular stroke work index, and right ventricular stroke work index initially increased to 221 +/- 12.5, 162 +/- 9.6, 142 +/- 11, and 203 +/- 29% but later fell to 169-173, 113-120, 69, and 148-117% of control, respectively. Heart rate initially rose to 145 +/- 5.9% and then stabilized at 160-162% of control. Pulmonary arterial occlusion pressure and central venous pressure initially fell to 82 +/- 8 and 93 +/- 9% but later rose to 87-102 and 105-120% of control levels, respectively. The hemodynamic response to severe heat stress in anesthetized humans was characterized by peripheral vasodilation accompanied by compensatory increases in heart rate and CI. Ventricular function, as reflected by SVI and CI, declined with continued heat stress, despite reduced afterload and stable or increased filling pressures. Pulmonary arterial temperature rose fastest, followed by the esophageal, rectal, and bladder temperatures, respectively. Jugular bulb temperature also rose rapidly.

Analysis of Variance↗
PubMed1999

Esophageal temperature threshold for sweating decreases before ovulation in premenopausal women.

The purpose of this study was to test the hypothesis that regulated body temperature is decreased in the preovulatory phase in eumenorrheic women. Six women were studied in both the preovulatory phase (Preov-2; days 9-12), which was 1-2 days before predicted ovulation when 17beta-estradiol (E2) was estimated to peak, and in the follicular phase (F; days 2-6). The subjects walked on a treadmill ( approximately 225 W x m-2) in a warm chamber (ambient temperature = 30 degreesC; dew-point temperature = 11.5 degreesC) while heavily clothed. E2, esophageal temperature (Tes), local skin temperatures, and local sweating rate were measured. The estimate of when the E2 surge would occur was correct for four of six subjects. In these four subjects, E2 increased (P </= 0.05) from 42.0 +/- 24.5 pg/ml during F to 123.2 +/- 31.3 pg/ml during Preov-2. Resting Tes was 37.02 +/- 0.20 degreesC during F and 36.76 +/- 0.28 degreesC during Preov-2 (P </= 0.05). The Tes threshold for sweating was decreased (P </= 0.05) from 36.88 +/- 0.27 degreesC during F to 36. 64 +/- 0.35 degreesC during Preov-2. Both mean skin and mean body temperatures were decreased during rest in Preov-2 group. The hypothesis that regulated body temperature is decreased during the preovulatory phase is supported.

Adult↗
PubMed2001

Influence of isometric exercise on blood flow and sweating in glabrous and nonglabrous human skin.

The distribution of the reflex effects of isometric exercise on cutaneous vasomotor and sudomotor function is not clear. We examined the effects of isometric exercise by different muscle masses on skin blood flow (SkBF) and sweat rate (SR) in nonglabrous skin and in glabrous skin. The latter contains arteriovenous anastomoses (AVAs), which cause large fluctuations in SkBF. SkBF was measured by laser-Doppler flowmetry (LDF) and reported as cutaneous vascular conductance (CVC; LDF/mean arterial pressure). SR was measured by capacitance hygrometry. LDF and SR were measured at the sole, palm, forearm, and ventral leg during separate bouts of isometric handgrip (IHG) and isometric leg extension (ILE). CVC and its standard deviation decreased significantly during IHG and ILE in the palm and sole (P < 0.05) but not in the forearm or leg (P > 0.05). Only palmar SR increased significantly during IHG and ILE (P < 0.05). We conclude that the major reflex influences of isometric exercise on the skin include AVAs and palmar sweat glands and that this is true for both arm and leg exercise.

Adult↗
PubMed2002

Role of skin blood flow and sweating rate in exercise thermoregulation after bed rest.

Two potential mechanisms, reduced skin blood flow (SBF) and sweating rate (SR), may be responsible for elevated intestinal temperature (T(in)) during exercise after bed rest and spaceflight. Seven men underwent 13 days of 6 degrees head-down bed rest. Pre- and post-bed rest, subjects completed supine submaximal cycle ergometry (20 min at 40% and 20 min at 65% of pre-bed rest supine peak exercise capacity) in a thermoneutral room. After bed rest, T(in) was elevated at rest (+0.31 +/- 0.12 degrees C) and at the end of exercise (+0.33 +/- 0.07 degrees C). Percent increase in SBF during exercise was less after bed rest (211 +/- 53 vs. 96 +/- 31%; P < or = 0.05), SBF/T(in) threshold was greater (37.09 +/- 0.16 vs. 37.33 +/- 0.13 degrees C; P < or = 0.05), and slope of SBF/T(in) tended to be reduced (536 +/- 184 vs. 201 +/- 46%/ degrees C; P = 0.08). SR/T(in) threshold was delayed (37.06 +/- 0.11 vs. 37.34 +/- 0.06 degrees C; P < or = 0.05), but the slope of SR/T(in) (3.45 +/- 1.22 vs. 2.58 +/- 0.71 mg x min-1 x cm-2 x degrees C-1) and total sweat loss (0.42 +/- 0.06 vs. 0.44 +/- 0.08 kg) were not changed. The higher resting and exercise T(in) and delayed onset of SBF and SR suggest a centrally mediated elevation in the thermoregulatory set point during bed rest exposure.

Adult↗
PubMed2005

Ten-day endurance training attenuates the hyperosmotic suppression of cutaneous vasodilation during exercise but not sweating.

It is well known that hyperosmolality suppresses thermoregulatory responses and that plasma osmolality (P(osmol)) increases with exercise intensity. We examined whether the decreased esophageal temperature thresholds for cutaneous vasodilation (TH(FVC)) and sweating (TH(SR)) after 10-day endurance training (ET) are caused by either attenuated increase in P(osmol) at a given exercise intensity or blunted sensitivity of hyperosmotic suppression. Nine young male volunteers exercised on a cycle ergometer at 60% peak oxygen consumption rate (V(O2 peak)) for 1 h/day for 10 days at 30 degrees C. Before and after ET, thermoregulatory responses were measured during 20-min exercise at pretraining 70% V(O2 peak) in the same environment as during ET under isoosmotic or hyperosmotic conditions. Hyperosmolality by approximately 10 mosmol/kgH2O was attained by acute hypertonic saline infusion. After ET, V(O2 peak) and blood volume (BV) both increased by approximately 4% (P < 0.05), followed by a decrease in TH(FVC) (P < 0.05) but not by that in TH(SR). Although there was no significant decrease in P(osmol) at the thresholds after ET, the sensitivity of increase in TH(FVC) at a given increase in P(osmol) [deltaTH(FVC)/deltaP(osmol), degrees C x (mosmol/kgH2O)(-1)], determined by hypertonic infusion, was reduced to 0.021 +/- 0.005 from 0.039 +/- 0.004 before ET (P < 0.05). The individual reductions in deltaTH(FVC)/deltaP(osmol) after ET were highly correlated with their increases in BV around TH(FVC) (r = -0.89, P < 0.005). In contrast, there was no alteration in the sensitivity of the hyperosmotic suppression of sweating after ET. Thus the downward shift of TH(FVC) after ET was partially explained by the blunted sensitivity to hyperosmolality, which occurred in proportion to the increase in BV.

Adaptation, Physiological↗
PubMed2002

Cholinergic urticaria, a new pathogenic concept: hypohidrosis due to interference with the delivery of sweat to the skin surface.

BACKGROUND: Acetylcholine has been suspected to be a pathogenetic factor for cholinergic urticaria (CU), without definite evidence. In contrast, there are scattered reports of CU associated with acquired generalized hypohidrosis. We have recently examined 2 patients with CU in both of whom we noticed the presence of extensive hypohidrosis that occurred only in winter. OBJECTIVE: In these 2 patients, acquired hypohidrosis due to superficial obstruction of the acrosyringium was suspected as the cause. Both case 1, a 22-year-old Japanese man, and case 2, a 21-year-old Japanese man, began to have anhidrosis and numerous red macules on their body whenever they felt hot in winter. These symptoms ceased to appear in summer. METHODS: We studied histologically their lesional skin in addition to provocation tests for CU. RESULTS: The diagnosis of CU was confirmed by the provocation of typical wheals after physical exercise in both cases. Histological study revealed findings suggestive of the presence of occlusion of the superficial acrosyringium. CONCLUSION: We think that such a hypohidrosis due to occlusion of superficial sweat ducts may also play a role in many other patients with CU of unknown etiology that becomes exacerbated in winter when sweating is not a frequent event.

Acetylcholine↗
PubMedDate not supplied

Increased sweat sodium concentration in patients with Alzheimer's disease.

Sweat sodium concentration was estimated with pilocarpine iontophoresis in 15 women with Alzheimer's disease (AD) and 29 healthy control women. The age ranged from 76 to 96 years with a mean age of 85 years in both groups. The mean sodium concentration of 91 +/- 41 mmol/l (n = 11) in the Alzheimer patients was significantly higher than in the control group (62 +/- 29 mmol/l, n = 27, p = 0.0011). 27% of AD patients and 7% of the control women did not respond to stimulation. The impaired sweating in AD patients make them more vulnerable to heat stress. Further studies are needed to reveal whether the neurophysiological mechanism involved is located in the hypothalamus in cortical projections to the hypothalamus or in postganglionic sympathetic fibers.

Aged↗
PubMed1977

Atypical sweat duct hyperplasia accompanying keratoacanthoma.

25 cases of atypical sweat duct proliferation in association with cutaneous tumors are described. 20 of these were keratoacanthomas. The compression of the duct either in its dermal or intraepidermal portion is considered to be the etiology. Similar changes are seen with decubitus ulcer and stasis dermatitis. Atypical sweat duct hyperplasia may be useful as an extra aid in the differentiation of keratoacanthoma from well-differentiated squamous cell carcinoma.

Carcinoma, Squamous Cell↗
PubMed1989

Interpretation of sweat sodium results--the effect of patient age.

In a retrospective study of sweat tests performed on 650 patients, sweat sodium was shown to increase with age in children without cystic fibrosis. The clearest separation of children with and without cystic fibrosis was in the youngest infants, while the highest proportion of repeatedly equivocal results was in the older children. Applying age-related reference ranges did not resolve the equivocal cases without also missing some cases of cystic fibrosis.

Age Factors↗
PubMed1991

Adenoid cystic carcinoma of sweat glands: report of two cases.

Two cases of primary cutaneous adenoid cystic carcinoma (ACC) of sweat gland origin are reported. The patients were a 83-year-old man and a 40-year-old woman. Histologically, the neoplasms showed the classic appearance of ACC. CEA, actin and S-100 protein were immunocytochemically demonstrated to be contained in some neoplastic cells. The literature on sweat gland ACC is reviewed and the clinicopathologic profile of this rare tumor considered.

Adult↗
PubMed1988

Metastatic sweat gland carcinoma in an adolescent: a case report.

Sweat gland carcinomas are rare tumors that metastasize frequently. The diagnosis is seldom suspected prior to histologic examination. A long interval between onset of the disease and diagnosis is characteristic of the disorder. The benign clinical and histologic appearance of some of these tumors can obscure their full malignant potential. This report illustrates an unusual instance of sweat gland carcinoma metastatic to bone carcinoma in an adolescent. This case stresses the necessity for those involved in the care of the foot to be familiar with a condition of this type.

Adenocarcinoma↗
PubMed1989

Localization of prolactin-like immunoreactivity in grafted human sweat glands.

Using a double-antibody immunoperoxidase technique, we demonstrated human prolactin-like material in some cells of the secretory coil and in luminal duct cells of sweat glands of human skin which had been carried as grafts on mice for 32-35 weeks. It therefore seems likely that a population of cells in the secretory coil synthesizes prolactin and can be considered as diffuse peripheral endocrine cells. The prolactin may function locally to regulate sweat electrolyte concentration.

Animals↗
PubMed1990

Localization of gamma-glutamyl transpeptidase in human sweat glands: an immunohistochemical study using a monoclonal antibody.

We studied the distribution of gamma-glutamyl transpeptidase (gamma-GT) by use of a monoclonal antibody (MAb) against human kidney gamma-GT in human sweat glands. In the eccrine sweat gland, the enzyme was localized along the luminal membrane and small apocrine extrusions of the superficial cells of the secretory portion. The intercellular canaliculi between basal cells were occasionally immunoreactive. In the secretory portion of the apocrine gland, luminal membrane and apocrine extrusions of various sizes and stages at the apices of the secretory cells exhibited positive reactions. Immunoreaction was also seen in the Golgi area of the cuboidal secretory cells. No positive reaction was observed in the myoepithelial cells of either gland or in the excretory duct cells.

Adult↗
PubMed1982

Pharmacological responsiveness of sweat glands in anxious patients and healthy volunteers.

The responsiveness of eccrine sweat glands to local intradermal injections of carbachol and phenylephrine was studied in six male and six female healthy volunteers and six female patients suffering from anxiety neurosis, using a plastic paint impression method. Carbachol evoked consistently greater responses than phenylephrine. The response to carbachol attained a peak approximately two minutes after injection, whereas the response to phenylephrine attained a peak within fifteen seconds of the injection. Males showed greater responsiveness to both drugs than females, this being reflected in significantly higher maxima of the dose-response curves for the males. The anxious females showed a higher level of spontaneous sweat gland activity and greater responsiveness to both drugs (reflected in higher maxima of the dose-response curves) than the normal females.

Adult↗