Local skin temperature alters cutaneous vasoconstrictor responses to a simulated hemorrhagic challenge while heat stressed

Tolerance to simulated hemorrhage is reduced with hyperthermia, due in part to inadequate cutaneous vasoconstriction. It is unclear how elevated skin temperatures, as experienced by soldiers on active duty, influence cutaneous vasoconstriction during simulated hemorrhage. 8 healthy males (34 ± 9 yr, 80.2 ± 4.2 kg) underwent a simulated hemorrhagic challenge via lower body negative pressure (LBNP) to pre‐syncope while heat stressed sufficient to increase core (Tcore Δ1.2 ± 0.2°C) and mean skin temperatures (Tsk mean 38.2 ± 0.7°C). Local skin temperatures at three forearm sites were held at 35.2±0.6°C, 38.2±0.2°C and 41.3± 0.7°C throughout heat stress and LBNP. At pre‐syncope mean arterial pressure declined (74±6 to 53 ± 8 mmHg P < 0.0001) while mean Tsk (38.2±0.7°C; P = 0.92) and local Tsk (35.1±0.8; 38.3±0.3 and 41.5±0.6°C; P > 0.05) were unchanged relative to heat stress baseline (i.e., pre‐LBNP). The magnitude of reduction in cutaneous vascular conductance during the final 90 seconds of LBNP from heat stress baseline was influenced by local Tsk (8% at ~35°C; 3% at ~38°C and 2% at ~42°C; P < 0.0001). In hyperthermic individuals the extent of cutaneous vasoconstriction during a simulated hemorrhage is dependent on skin temperature. In situations where a soldier's skin temperature exceeds 38°C, cutaneous vasoconstriction to a hemorrhagic challenge is likely negligible. NIH HL61388 and HL84072