current CFDI technology enables a reproducible estimation of popliteal artery flow velocities. IPC(foot)can significantly augment arterial calf inflow on an acute basis both in normals and claudicants. The increase of EDV and decrease of PI indicate that attenuation of peripheral resistance to flow is the main mechanism underlying the popliteal artery vFl enhancement on application of IPC(foot). Prospective trials on the long-term effect of IPC(foot)in the management of patients with PVD are indicated from the results of this study.

all IPC modes proved effective, IPC(foot+calf)generating the highest venous outflow enhancement. Higher venous volumes expelled with IPC(foot+calf)explain its reported superiority on leg inflow over the other modes. Increase of applied pressure from 120 to 180 mmHg with IPC(foot)offered only a small outflow improvement. Venous haemodynamics at rest and with IPC in claudicants do not differ significantly from those in healthy subjects.

Patients with claudication had a significant impairment of orthostatic sympathetic autoregulation. After successful revascularization, and in spite of the extensive disease in the receiving circulation, this autoregulation returned to normal. Presented previously to the Vascular Surgical Society in London, November 1997 and published in abstract form as Br J Surg 1998; 85: 557

the striking similarity in the haemodynamic effects of IPC(foot)and postural alteration in the popliteal artery strongly suggests that the leg inflow enhancement with IPC(foot)is mediated by a transient suspension of peripheral sympathetic autoregulation. In addition to their role as clinical markers of PVD severity, the autoregulatory reflexes of peripheral circulation appear to have functions with significant clinical implications in the management of patients with leg inflow impairment.