抄録
Plasma hyperosmolality inhibits thermoregulatory responses during heat stress by elevating body core temperature (Tc) thresholds for cutaneous vasodilation (CVD) and sweating. To examine the role of vasoconstrictor system in the osmotic elevation of Tc threshold for CVD, we examined the effect of local bretylium treatment, which inhibits norepinephrine release from sympathetic nerve terminals, on cutaneous vascular response to passive body heating. Seven healthy male subjects were infused with either hypertonic (3% NaCl) or isotonic (0.9% NacCl) saline, and then passively heated by immersing their lower legs in 42 °C water for 60 min (room temperature, 28°C; RH, 40%). Bretylium tosylate was iontophoretically applied on forearm skin. We measured the skin blood flow by laser-Doppler flowmetery at the bretylium-treated and adjacent untreated sites, and deteremined the Tc (represented by esophageal temperature) threshold for CVD in each subject in each condition and treatment. Plasma osmolality was increased by 13 mOsm/kg H2O following hypertonic saline infusion, and was unchanged following isonotic saline. The Tc threshold for CVD was elevated by ~1.0°C following hypertonic saline infusion. This elevation was not influenced by treatment with bretylium. These results suggest that osmotically-induced elevation of body core temperature threshold for CVD is primarily due to inhibition of active vasodilation, but not due to the enhancement of vasoconstrictor system. [Jpn J Physiol 54 Suppl:S234 (2004)]
