Accumulation of FDG in axillary sweat glands in hyperhidrosis: a pitfall in whole-body PET examination

Each year millions of individuals sustain burns. Within the US 40,000–70,000 individuals are hospitalized for burn-related injuries, some of which are quite severe, requiring skin grafting. The grafting procedure disrupts neural and vascular connections between the host site and the graft, both of which are necessary for that region of skin to contribute to temperature regulation. With the use of relatively modern techniques such as laser-Doppler flowmetry and intradermal microdialysis, a wealth of information has become available regarding the consequences of skin grafting on heat dissipation and heat conservation mechanisms. The prevailing data suggest that cutaneous vasodilator capacity to an indirect heat stress (i.e., heating the individual but not the evaluated graft area) and a local heating stimulus (i.e., directly heating the graft area) is impaired in grafted skin. These impairments persist for ≥4 yr following the grafting procedures and are perhaps permanent. The capacity for grafted skin to vasodilate to an endothelial-dependent vasodilator is likewise impaired, whereas its capacity to vasodilate to an endothelial-independent vasodilator is generally preserved. Sweating responsiveness is minimal to nonexistent in grafted skin to both a whole body heat stress and local administration of the primary neurotransmitter responsible for stimulating sweat glands (i.e., acetylcholine). Likewise, there is no evidence that this absence of sweat gland responsiveness improves as the graft matures. In contrast to the heating stimuli, cutaneous vasoconstrictor responses to both indirect whole body cooling (i.e., exposing the individual to a cold stress but not at the evaluated graft area) and direct local cooling (i.e., directly cooling the graft area) are preserved in grafted skin as early as 5–9 mo postgrafting. If uninjured skin does not compensate for impaired heat dissipation of grafted skin, individuals having skin grafts encompassing significant fractions of their body surface area will be at a greater risk for a hyperthermic-related injury. Conversely, the prevailing data suggest that such individuals will not be at a greater risk of hypothermia upon exposure to cold environmental conditions.

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Features of transcutaneous penetration of lead into the human body

Hygiene and Sanitation ◽

10.47470/0016-9900-2021-100-1-55-59 ◽

2021 ◽

Vol 100 (1) ◽

pp. 55-59

Author(s):

Nikolay A. Kashuba

Keyword(s):

Physical Activity ◽

Particle Size ◽

Lactic Acid ◽

Human Body ◽

Inorganic Compounds ◽

The Body ◽

Whole Body ◽

Sweat Glands ◽

Mechanical Methods ◽

Intense Physical Activity

Introduction. One of the features of lead is its high ability to disintegrate and significantly contaminate the environment. The contamination of hands or the whole body with lead creates a high probability of penetrating micro- and nanoparticles through the skin into the body. Nowadays, this process is not sufficiently studied. There is evidence that inorganic compounds or metallic particles of lead can penetrate through the skin into a human body. Material and methods. centrifuge 10000 rpm, laser emitter (wavelength 625-740 nm), optical microscope, voltampermetric analyzer ABA-2, Analysette 12 Dyna Sizer, magnetic stirrer, distiller, Na2S solution. The studies were conducted in 2017-2018 among the workers of battery sections of technical service stations in Ternopol - 17 people. The research results were processed by the statistical package SPSS 19. Results. The process of mechanical contamination by the skin with lead, rejection of micro particles from the surface of lead, and, to a lesser extent, ultrafine nanoparticles, which can penetrate the sweat glands, was established to occur. The studies have shown in the washings from the palms particles’ skin are detected mainly in the size of 1 μm - 100 nm. In the process of finding the particles of lead in the sweat glands, their length decreases to Nanoscale, allowing them freely entering the body. The decrease in particle size in the sweat glands occurs due to the formation of soluble lead compounds. Presumably, the main chemical contributing to this process is lactic acid. With increasing exposure, the size of lead particles in the sweat glands decreases. Intensive cleaning of the skin surface by mechanical methods, and detergents, followed by contamination with lead, promotes the penetration of lead particles into the sweat glands and its further spread in the body. The intense physical activity was established to contribute to a decrease in particle size, which suggests chemical interaction of lead with lactic acid and the formation of soluble lead lactate. The assumption is confirmed by studies of the composition of sweat, which is detected lead lactate. Conclusion. The lead ability to penetrating a human body transcutaneously in the form of nanoparticles and soluble compounds has been proven. Intense physical activity facilitates the penetration of lead into the body.

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Skin tattooing impairs sweating during passive whole body heating

Journal of Applied Physiology ◽

10.1152/japplphysiol.00427.2019 ◽

2020 ◽

Vol 129 (5) ◽

pp. 1033-1038

Author(s):

Maurie J. Luetkemeier ◽

Dustin R. Allen ◽

Mu Huang ◽

Faith K. Pizzey ◽

Iqra M. Parupia ◽

...

Keyword(s):

Sweat Rate ◽

Whole Body ◽

Sweat Glands ◽

Moderate Increase ◽

The Novel ◽

Cholinergic Stimulation ◽

Whole Body Heat Stress ◽

Reflex Control ◽

Body Heat ◽

Eccrine Sweat Glands

This study is the first to assess the reflex control of sweating in tattooed skin. The novel findings are twofold. First, attenuated increases in sweat rate were observed in tattooed skin compared with adjacent healthy non-tattooed skin in response to a moderate increase (1.0°C) in internal temperature during a passive whole body heat stress. Second, reduced sweating in tattooed skin is likely related to functional damage to the secretory mechanisms of eccrine sweat glands, rendering it less responsive to cholinergic stimulation.

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Is active sweating during heat acclimation required for improvements in peripheral sweat gland function?

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00253.2009 ◽

2009 ◽

Vol 297 (4) ◽

pp. R1082-R1085 ◽

Cited By ~ 28

Author(s):

Michael J. Buono ◽

Travis R. Numan ◽

Ryan M. Claros ◽

Stephanie K. Brodine ◽

Fred W. Kolkhorst

Keyword(s):

Sweat Gland ◽

Sweat Rate ◽

Heat Acclimation ◽

Whole Body ◽

Moderate Intensity ◽

Sweat Glands ◽

Exercise Heart Rate ◽

Sweat Production ◽

Gland Function ◽

Pilocarpine Iontophoresis

We investigated whether the eccrine sweat glands must actively produce sweat during heat acclimation if they are to adapt and increase their capacity to sweat. Eight volunteers received intradermal injections of BOTOX, to prevent neural stimulation and sweat production of the sweat glands during heat acclimation, and saline injections as a control in the contralateral forearm. Subjects performed 90 min of moderate-intensity exercise in the heat (35°C, 40% relative humidity) on 10 consecutive days. Heat acclimation decreased end-exercise heart rate (156 ± 22 vs. 138 ± 17 beats/min; P = 0.0001) and rectal temperature (38.2 ± 0.3 vs. 37.9 ± 0.3°C; P = 0.0003) and increased whole body sweat rate (0.70 ± 0.29 vs. 1.06 ± 0.50 l/h; P = 0.030). During heat acclimation, there was no measurable sweating in the BOTOX-treated forearm, but the control forearm sweat rate during exercise increased 40% over the 10 days ( P = 0.040). Peripheral sweat gland function was assessed using pilocarpine iontophoresis before and after heat acclimation. Before heat acclimation, the pilocarpine-induced sweat rate of the control and BOTOX-injected forearms did not differ (0.65 ± 0.20 vs. 0.66 ± 0.22 mg·cm−2·min−1). However, following heat acclimation, the pilocarpine-induced sweat rate in the control arm increased 18% to 0.77 ± 0.21 mg·cm−2·min−1 ( P = 0.021) but decreased 52% to 0.32 ± 0.18 mg·cm−2·min−1 ( P < 0.001) in the BOTOX-treated arm. Using complete chemodenervation of the sweat glands, coupled with direct cholinergic stimulation via pilocarpine iontophoresis, we demonstrated that sweat glands must be active during heat acclimation if they are to adapt and increase their capacity to sweat.

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Effect of age on heat-activated sweat gland density and flow during exercise in dry heat

Journal of Applied Physiology ◽

10.1152/jappl.1987.63.3.1089 ◽

1987 ◽

Vol 63 (3) ◽

pp. 1089-1094 ◽

Cited By ~ 66

Author(s):

R. K. Anderson ◽

W. L. Kenney

Keyword(s):

Older Women ◽

Sweat Gland ◽

Age Groups ◽

Whole Body ◽

Moderate Intensity ◽

Exercise Session ◽

Sweat Glands ◽

Moderate Intensity Exercise ◽

Age Related ◽

Eccrine Glands

Physiological responses of eight postmenopausal older women (age 52–62 yr) and eight younger women (age 20–30 yr) were compared during moderate intensity exercise in a hot dry environment (48 degrees C dry bulb, 25 degrees C wet bulb). The age groups were matched on the basis of maximal O2 consumption (VO2max), body surface area, and body fatness. After heat acclimation the women walked at 40% VO2max for up to 2 h in the hot dry environment while heart rate (HR), rectal temperature (Tre), mean skin temperature (Tsk), whole-body sweating rate (Msw), and local sweating rates (msw; forearm, chest, and scapula) were measured. Additionally, the density of heat-activated sweat glands (HASG) was determined and average sweat gland flow (SGF) was calculated for the scapular area. Although no differences between age groups were found in HR response (when analyzed as percent of maximal HR) or Tsk, the older women had a significantly higher Tre throughout the heat-exercise session. The greater heat storage of the older women may be explained by their significantly lower Msw and msw. There were no differences between the younger and older women in the density of HASG after 30 min; therefore, the lower msw reflects a diminished output per HASG rather than a decrease in the number of sweat glands recruited. The diminished thermoregulatory ability of the older women, unrelated to differences in VO2max, appears to reflect either 1) a diminished response of the sweat glands to central and/or peripheral stimuli, or 2) an age-related structural alteration in the eccrine glands or surrounding skin cells.

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