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1 ased internal temperature (> 1.0 degrees C), cutaneous vascular conductance (approximately fivefold),
6 der (60 +/- 6 years) males (nine per group), cutaneous vascular conductance (CVC) and sweat rate were
7 ta were expressed as a percentage of maximal cutaneous vascular conductance (CVC) at each site (28 mm
8 essure (MAP) was measured non-invasively and cutaneous vascular conductance (CVC) calculated as LDF/M
14 monitored using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated (las
16 was used as an index of skin blood flow and cutaneous vascular conductance (CVC) was calculated as L
17 telemetric pill were measured continuously; cutaneous vascular conductance (CVC) was calculated as l
18 as measured via laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated as R
19 The NO component of the heat-induced rise in cutaneous vascular conductance (CVC) was diminished in t
25 (FVC, venous occlusion plethysmography) and cutaneous vascular conductance (CVC, laser-Doppler) were
28 ured using laser-Doppler flowmetry (LDF) and cutaneous vascular conductance (CVC; LDF/mean arterial p
29 es show that the rise in skin blood flow and cutaneous vascular conductance during heat stress is sub
31 n; P=0.66), whereas the elevation in forearm cutaneous vascular conductance in patients with CHF was
32 infusion of HYPER saline increased baseline cutaneous vascular conductance (P </= 0.01), which did n
35 lux (LDF) was measured over each MD site and cutaneous vascular conductance was calculated as CVC = L
37 eek intervention period in the uncuffed arm (cutaneous vascular conductance week 0 vs. week 4 at 41 d
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