Low pressure venous return results from several different pump systems
. Blood flow and velocity depend on sympathetic tone and contraction o
f the veins modulating distensibility. In patients with chronic venous
insufficiency, different components including hyperdistensibility, hy
perpressure, valve failure, back-flow and stasis, lead to a vicious ci
rcle. These elements modify the venous wall and lead to hyperdistensio
n producing modified distensibility and/or formation of varicose veins
. Endothelial and smooth muscle cells participate in these changes. Sm
ooth muscle cells play a major role: some hypertrophy and/or lose thei
r contractility, synthesizing and some times rapidly destroying tissue
. These changes in the circulation, sometimes increased by inflammatio
n and thrombosis, affect microcirculatory haemodynamics with a variabl
e delay. The venous system, even when pathological (as long as it is n
ot totally invaded by fibrosis) responds to a large number of relaxing
or constricting pharmacological agents, justifying their therapeutic
value.