When venous pressure in the human lower limb was raised by application of small cumulative pressure increases to a venous congestion cuff, Gamble et al. (1998) observed, using strain gauge plethysmography and arterial Doppler ultrasound, that arterial inflow to the limb remained constant even at congestion pressures approaching mean arterial pressure. They attributed this to a progressive reduction in pre-capillary resistance due to retrograde veni-arteriolar transmission of vasodilatory signals via the endothelium. This idea was supported by their subsequent finding that in pre-eclampsia, a condition characterised by dysfunction of the endothelium, calf blood flow decreased during venous congestion (Anim-Nyame et al. 2003). Since vascular control mechanisms in skin and skeletal muscle within a whole limb differ, we studied whether retrograde transmission is evident in the former during a venous congestion protocol.

With approval from the University of Birmingham Local Ethics committee, 8 healthy males, aged 26 ± 1 years (mean ± S.E.M.), with resting mean arterial pressures (MAP) of 82 ± 2 mmHg and heart rates 56 ± 2 beats per min, participated in the study. Calf blood flow was measured by strain gauge plethysmography (Filtrass 2000, DOMED) and skin perfusion by Laser Doppler probes on the shin and foot dorsum during supine rest and at the end of 5 min periods of venous congestion by a thigh cuff inflated successively to 10, 20, 30, 40 and 50 mmHg. Blood flow measurements were made by brief (10 s cuff inflations to 40-50 mmHg above pre-existing cuff pressure. Blood flows and averaged arbitrary perfusion values for shin and foot during venous congestion were expressed relative to rest values.

Skin perfusion declined steadily as venous congestion increased, reaching 39 ± 3 % of resting at 50 mmHg cuff pressure. The decrease was no different than predicted by Darcy’s Law based on the rise in venous pressure. Calf blood flow at rest was 2.17 ± 0.83 mls min^-1 100 ml^-1 and as venous congestion increased in steps, it remained unchanged up to 30 mmHg (105 ± 12 % of resting). At 40 and 50 mmHg congestion pressures, calf flows were reduced to 75 ± 10 % and 60 ± 6 % of resting (P < 0.05, paired t test), most likely because the thigh cuff pressure used to measure flow exceeded MAP.

We conclude that a protocol of small cumulative increases in venous pressure does not invoke retrograde transmission of vasodilatory signals in skin. Where such a protocol shows whole limb blood flow to be reduced, impairment of signal transmission is more likely to reside in other tissues such as skeletal muscle.