Modification of Cutaneous Vasodilator System during Heat Stress by Increased Plasma Osmolality

Abstract

0270 Increased plasma osmolality inhibits cutaneous vasodilation by elevating the internal temperature threshold for cutaneous vasodilation during heat stress. However, it is not clear whether the effect of hyperosmolality on the cutaneous circulatory response to heat stress is via the adrenergic vasoconstrictor system or the non-adrenergic active vasodilator system. PURPOSE: This study was designed to find the contribution of the vasoconstrictor and active vasodilator systems to the inhibition of the cutaneous vasodilation by increased plasma hyperosmolality. METHODS: Skin blood flow was monitored at control sites and at sites pretreated with bretylium (BT) by iontophoresis to block vasoconstrictor nerve function. Healthy male subjects were infused with either isotonic (0.9% NaCl) or hypertonic (3% NaCl) saline for 90 min on separate day. Following a 30-minute resting period after the end of infusion, subjects were passively heated by immersing their lower legs into hot water at 42°C (room temperature 25°C) for 60 min. RESULTS: The increase in esophageal temperature during hot water leg-immersion was greater in hyperosmotic conditions relative to normosmotic conditions (P<0.05) although resting esophageal temperature was not different between conditions. The esophageal temperature threshold for cutaneous vasodilation was significantly shifted to higher internal temperatures in hyperosmotic conditions compared with thresholds observed in normosmotic conditions at both control (P<0.05) and BT treated sites (P<0.05). CONCLUSIONS: These results indicate hyperosmotic inhibition of the reflex thermoregulatory control of skin blood flow durign passive heat stress is through the active vasodilator system.