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Eight healthy participants (four men and four women; 32 �� 7 years old; 75.2 �� 10.8 kg) underwent lower-body negative pressure to presyncope while heat stressed via a water-perfused suit sufficiently to increase core temperature by 1.2 �� 0.2��C. At forearm skin sites distal to the water-perfused suit, local skin Osimertinib manufacturer temperature was either 35.2 �� 0.6 (mild heating) or 38.2 �� 0.2��C (moderate heating) throughout heat stress and lower-body negative pressure, and remained at these temperatures until presyncope. The reduction in cutaneous vascular conductance during the final 90 s of lower-body negative pressure, relative to heat-stress baseline, was greatest at the mildly heated site (?10 �� 15% reduction) relative to GPX4 the moderately heated site (?2 �� 12%; P= 0.05 for the magnitude of the reduction in cutaneous vascular conductance between sites), because vasoconstriction at the moderately heated site was either absent or negligible. In hyperthermic individuals, the extent of cutaneous vasoconstriction during a simulated haemorrhage can be modulated by local skin temperature. In situations where skin temperature is at least 38��C, as is the case in soldiers operating in warm climatic conditions, a haemorrhagic insult is unlikely to be accompanied by cutaneous vasoconstriction. Compared with normothermia, hyperthermic individuals develop syncopal symptoms much sooner during upright tilt and lower-body negative pressure (LBNP), as evidenced by an earlier incidence of hypotension (Johnson et al. 1973; Keller et al. 2009) and reductions in cerebral blood velocity, indicating reductions in cerebral perfusion (Wilson et al. 2006). Cutaneous vasodilatation during whole-body heat stress is the primary mechanism for reductions in systemic vascular resistance (Rowell et al. Alectinib mouse 1969) and central blood volume (Crandall et al. 2008, 2012). In normothermic humans, skin blood flow is relatively low, and thus reductions in cutaneous vascular conductance will likely exert no more than minimal influences on arterial blood pressure. However, with profound heat-induced increases in cutaneous vascular conductance, resulting in as much as 7 l min?1 blood flow through the skin (Rowell, 1986), subsequent cutaneous vasoconstriction has the potential to increase mean arterial pressure significantly, which would be beneficial in preserving tolerance to a hypotensive challenge. Whole-body heat stress is often evoked via perfusing hot water through a tube-lined suit worn by the subject, which typically increases skin temperature under the suit to ��38��C. Notably, most studies of this type evaluate cutaneous vascular responses from an area (e.g. forearm) that is not exposed to this elevated temperature.