Abstract Experiments were performed in chloralose anesthetized dogs to test if the saphenous vein (a cutaneous vein) participates in the cardiovascular response to systemic hypoxemia. The saphenous vein was perfused at constant flow with cooled blood (32°C) from the terminal aorta. Sixteen paralyzed (gallamine triethiodide) animals were ventilated with 10% O 2 in N 2 for 4-min episodes; arterial PO 2 was 49 ± 4 mm Hg after 4 min of ventilation with this gas mixture. Hypoxemia caused a 29% decrease in saphenous vein perfusion pressure (interpreted as a dilation) and an 8% increase in aortic pressure. The hypoxemia induced saphenous venous dilation was abolished by (1) section of the vagus nerves and denervation of the carotid chemoreceptors (afferent pathways), or (2) section of the lumbar sympathetic chain (efferent pathway). These data demonstrate that systemic hypoxemia causes a neurally mediated dilation of the saphenous vein that is dependent upon intact carotid chemoreceptors and/or vagus nerves. It is concluded that saphenous vein dilation is part of the integrated cardiovascular response to hypoxemia in anesthetized dogs. This reflex effect may represent a decompensatory mechanism that compromises cardiac output during hypoxemia in animals with hypothermic extremities.