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01. There was a significant interaction for cutaneous vascular conductance between sites and the final 90 s of LBNP (P= 0.007), demonstrating GPX4 that the magnitude of the change in cutaneous vascular conductance during LBNP was affected by site temperature. Consistent with that observation, at presyncope cutaneous vascular conductance decreased by 10 �� 15% at the mild site (Fig. 3), while it was unchanged at the moderate site (?2 �� 12 conductance units; P= 0.05 between sites). The primary aim of this project was to investigate whether, during a whole-body heat stress, a local skin temperature comparable to the mean skin temperature under the water-perfused suit (i.e. 38��C) attenuates the magnitude of cutaneous vasoconstriction in response to a simulated haemorrhagic challenge. To address this hypothesis, local skin temperature was either allowed to increase as it normally would at a non-heated forearm site or locally heated to a level comparable to mean skin temperature under the water-perfused suit, while cutaneous vasoconstrictor responses at both sites were evaluated during a subsequent simulated haemorrhagic challenge. This experimental model allowed for the examination of cutaneous vascular responses to neurally mediated vasoconstriction across two different skin temperatures, thereby providing insight into the cutaneous vascular responses in the vast majority of skin (i.e. under the water-perfused suit) during a hypotensive challenge in heat-stressed Osimertinib price humans. The findings demonstrate that the magnitude of cutaneous vasoconstriction during a simulated haemorrhagic find more challenge is attenuated in skin heated to 38��C. This observation suggests that hyperthermic humans experiencing a hypotensive insult are unlikely to vasoconstrict the cutaneous circulation in areas where local skin temperature is ��38��C. In heat-stressed humans cardiac output can increase upwards to 13 l min?1 (Rowell, 1986), of which up to 50% is directed towards cutaneous vascular beds (Rowell et al. 1969). Given the profound increases in cutaneous vascular conductance in these conditions, adequate control of cutaneous vascular tone is essential for the maintenance of arterial blood pressure during a subsequent hypotensive challenge (Rowell et al. 1973; Tripathi & Nadel, 1986; Kellogg et al. 1990). At such high vascular conductances, reductions in cutaneous vascular conductance will help maintain arterial blood pressure in the face of the hypotensive challenge. For example, we have shown that cutaneous vasoconstriction associated with skin cooling of heat-stressed subjects increases cerebral blood velocity and improves orthostatic tolerance relative to heat stress alone (Wilson et al. 2002). However, despite a profound hypotensive state, there was little to no reduction in cutaneous vascular conductance in skin locally heated to 38��C (Fig. 3).