Microvessels, especially in the skin and muscles are organized in func
tional units. These units are controlled by the adrenergic system and
hormones but also have autonomous metabolic and myogenic regulatory sy
stems independent of vasomotion. Microcirculatory blood flow is affect
ed by special theologic properties: a low arteriolar haematocrit rises
to the systemic level in the venules. The flow rate in the venules is
low, and together with the raised haematocrit, explains the microvenu
lar sensitivity to hyperviscosity. Capillarovenular microangiopathy, r
ecently described by standard and fluorescent capillaroscopy, develops
during chronic venous insufficiency. The capillary loops appear dilat
ed and knotted together with fibrous deposits and pericapillary oedema
. Venous hyperpressure is the cause of this microangiopathy. Together
these phenomena disrupt normal haemodynamics and physiology of the mic
rocirculatory unit: baseline hyperhaemia, lowered vasomotor and vasomo
tion reactivity, development of theologic disorders (haemoconcentratio
n, hyperfibrinogenaemia, erythrocyte agregation) and decreased fibrino
lysis. Modifications in the transcapillary exchange is related to hypo
xia and is aggravated by depressed lymphatic drainage. The main conseq
uence is oedema. Inflammation, a characteristic of these microangiopat
hies could occur when the endothelium is activated by the hypoxia. The
classical mediators of inflammation would activate interactions betwe
en the different cells: endothelium, granulocytes, monocytes and plate
lets. Several pharmacological models have been developed for the analy
sis of these data including exploration of the permeability and capill
ary resistance and theological analysis. Objective observation of the
microangiopathy with capillaroscopy, together with modern haemodynamic
al, biological and pharmacological methods are essential for a better
understanding of microvascular disorders in chronic venous insufficien
cy.