The PO2 in the lumen and valve pockets of veins in 2 patients and 8 dogs was measured during streamline blood flow and in conditions of intermittent pulsatile flow. The blood within the valve pockets became rapidly hypoxic when undisturbed during streamline flow (i.e. when "static"), but the PO2 in the pockets rose to that of the lumenal blood when the column of venous blood was made to pulsate and so empty the valve pockets at short intervals. The observations suggest that the endothelium covering the valve cusps is entirely dependent on pocket or lumenal blood for its oxygen supply. The endothelium facing the pocket can therefore become hypoxic during non-pulsatile blood flow when that facing the lumen is adequately to oxygenated. Early thrombus formation was seen to develop on a valve cusp after only 2 h non-pulsatile flow. The demonstration that localized hypoxaemia occurs readily and can produce endothelial damage, in circumstances and situations where thrombi are commonly found to originate, is additional circumstantial evidence that hypoxia may trigger thrombogenesis.