Thermoregulatory vasodilation increases the venous partial pressure of oxygen

Thermoregulatory arteriovenous shunt vasoconstriction may facilitate deep-vein thrombosis by producing relative venous stasis and hypoxia. Accordingly, we evaluated the effect of vasomotion on leg blood flow and venous oxygen tension. We studied five male volunteers, each of whom was warmed enough to trigger vasodilation and then cooled sufficiently to provoke thermoregulatory vasoconstriction. The process was then repeated during N2O/desflurane anesthesia. Venous oxygen tension and saturation (with a fraction of inspired oxygen of 1.0) were evaluated in blood samples taken from a catheter that was inserted into a saphenous vein at the ankle and advanced until the tip was proximal to the knee. Thermoregulatory vasodilation with or without general anesthesia significantly increased arteriovenous shunt flow by approximately 10-fold, and increased total leg flow approximately sixfold. However, vasodilated flows were similar with and without general anesthesia, as were vasoconstricted flows. Before induction of anesthesia, thermoregulatory vasodilation increased venous oxygen tension from 46 +/- 6 to 187 +/- 99 mm Hg and venous saturation from 79% +/- 6% to 99% +/- 2%. After induction of anesthesia, thermoregulatory vasodilation increased venous oxygen tension from 55 +/- 11 to 356 +/- 103 mm Hg and venous saturation from 84% +/- 8% to 100% +/- 0%. Our data thus indicate that thermoregulatory vasodilation markedly increases both leg flow and venous oxygenation; and that both factors may help prevent perioperative venous thrombosis.

Thermoregulatory arteriovenous shunt vasoconstriction may facilitate deep-vein thrombosis by producing related venous stasis and hypoxia. In male volunteers, the authors found that when vasodilation induced by warming was produced, both blood flow and venous oxygenation increased, both of which may help prevent perioperative venous thrombosis.