Neural control of cutaneous vasoconstriction during lower‐body negative pressure (LBNP) in the heat stressed individual

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The decrease in cutaneous vascular conductance (CVC) during LBNP in the heat stressed human could be mediated by neural and non‐neural mechanisms. This project further investigated this question. Nerve activity to a forearm was blocked (via axial blockade) in seven healthy subjects. Two intradermal microdialysis probes were placed within the skin of the blocked area. Forearm skin blood flow was measured by laser‐Doppler flowmetry over these microdialysis probes, as well as from skin of the contralateral (non‐blocked) forearm. The absence of sweating and cutaneous vasodilation during heat stress confirmed an effective block. Upon this confirmation, adenosine was perfused through one microdialysis probe to increase skin blood flow similar to that of the non‐blocked site. After internal temperature was elevated ~1.0 °C, 30 mmHg LBNP was applied for 10 min, or until the onset of presyncopal symptoms. LBNP significantly decreased CVC at all three sites (unblocked site: −6.1±2.7; blocked site: −2.5±1.3%max; blocked site with adenosine: −5.4±2.2%max), although the magnitude of reduction in CVC was not different between unblocked and adenosine sites. When combined with prior data, these findings suggest that reductions in CVC to LBNP of heat stressed individuals could have both neural and non‐neural components.Study funded by part by NIH HL61388 & HL84072