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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
11 us system activity (SSNA) or its relation to cutaneous vascular conductance (CVC) during passive heat
15 monitored using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated (las
16 telemetric pill were measured continuously; cutaneous vascular conductance (CVC) was calculated as l
18 was used as an index of skin blood flow and cutaneous vascular conductance (CVC) was calculated as L
19 as measured via laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated as R
20 The NO component of the heat-induced rise in cutaneous vascular conductance (CVC) was diminished in t
26 (FVC, venous occlusion plethysmography) and cutaneous vascular conductance (CVC, laser-Doppler) were
29 ured using laser-Doppler flowmetry (LDF) and cutaneous vascular conductance (CVC; LDF/mean arterial p
31 es show that the rise in skin blood flow and cutaneous vascular conductance during heat stress is sub
32 skin sympathetic outflow or its relation to cutaneous vascular conductance during heat stress is unk
34 n; P=0.66), whereas the elevation in forearm cutaneous vascular conductance in patients with CHF was
36 infusion of HYPER saline increased baseline cutaneous vascular conductance (P </= 0.01), which did n
39 lux (LDF) was measured over each MD site and cutaneous vascular conductance was calculated as CVC = L
41 eek intervention period in the uncuffed arm (cutaneous vascular conductance week 0 vs. week 4 at 41 d