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Histamine receptor antagonists have the capacity to alter in vivo human sweating: implications for hypohidrosis
Author(s) -
Wilson Thad E.,
Meade Stephanie,
Stump Corey,
Skaggs Kendra,
Banwait Sumeet,
Galloway Samantha,
Garrett Jason
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.842.11
Subject(s) - pyrilamine , microdialysis , histamine , medicine , sweat , perfusion , anesthesia , heart rate , forearm , chemistry , antagonist , receptor , blood pressure , surgery , central nervous system
An atopic dermatitis mouse model has identified histamine and the histamine type‐1 receptor (H1R) pathway to be a mechanism of disease‐induced hypohidrosis. To begin to translate these findings into in vivo human skin, we tested the hypothesis that intradermal perfused H1R antagonist pyrilamine maleate would accentuate local eccrine sweating induced sympathetically via whole‐body heat stress. Two intradermal microdialysis probes were placed into the dorsal forearm of 3 healthy female and 2 healthy male subjects (health determined by health history and physical exam; age = 25±1 yrs; and BMI = 25.3±3.5 kg/m 2 ) to perfuse (5 μL/min) of pyrilamine maleate (3 mM) or the vehicle (lactated Ringer's) while measuring sweat rate (capacitance hygrometry) directly over the microdialysis membrane. Whole body heating (46°C water perfusion of a high‐density tube‐lined suit) increased intestinal temperature (pill telemetry) by 1.0°C from 36.9±0.2°C, heart rate (ECG) by 32±5 bpm, calf blood flow (venous occlusion plethysmography) by 7.8±1.4 ml/100 ml tissue, and whole‐body sweat loss of 1.5±0.2 kg but did not significantly alter mean arterial pressure. Mean skin temperature was clamped under the suit at 38–39°C, while uncovered forearm skin temperature increased from 29.6±0.3 to 35.1±0.6°C. Pyrilamine maleate increased local sweat rate compared to the vehicle control beginning at 35 min of whole‐body heating (intestinal temperature of 37.1±0.2°C) and this difference remained throughout the heat stress (group: P=0.008, time: P<0.001, and interaction: P<0.001). These data indicate that the H1R mechanism has the capacity to alter sweat rate during a physiological induced sudorific perturbation known to affect histamine concentration in human skin. Thus, it is possible that this mechanism of hypohydrosis could be a viable target in individuals with atopic dermatitis. Support or Funding Information Laboratory support: NIH AR069912 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .