title: [Microcirculation and rheology].
abstract: Microvessels, especially in the skin and muscles are organized in functional units. These units are controlled by the adrenergic system and hormones but also have autonomous metabolic and myogenic regulatory systems independent of vasomotion. Microcirculatory blood flow is affected by special rheologic 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 microvenular sensitivity to hyperviscosity. Capillarovenular microangiopathy, recently described by standard and fluorescent capillaroscopy, develops during chronic venous insufficiency. The capillary loops appear dilated 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 microcirculatory unit: baseline hyperhaemia, lowered vasomotor and vasomotion reactivity, development of rheologic disorders (haemoconcentration, hyperfibrinogenaemia, erythrocyte agregation) and decreased fibrinolysis. Modifications in the transcapillary exchange is related to hypoxia and is aggravated by depressed lymphatic drainage. The main consequence is oedema. Inflammation, a characteristic of these microangiopathies could occur when the endothelium is activated by the hypoxia. The classical mediators of inflammation would activate interactions between the different cells: endothelium, granulocytes, monocytes and platelets. Several pharmacological models have been developed for the analysis of these data including exploration of the permeability and capillary resistance and rheological analysis. Objective observation of the microangiopathy with capillaroscopy, together with modern haemodynamical, biological and pharmacological methods are essential for a better understanding of microvascular disorders in chronic venous insufficiency.
authors.affiliation: Sanofi Recherche, Montpellier.
authors.forename: A
authors.initials: A
authors.lastname: Barbier
authors.forename: M R
authors.initials: MR
authors.lastname: Boisseau
authors.forename: P
authors.initials: P
authors.lastname: Braquet
authors.forename: P
authors.initials: P
authors.lastname: Carpentier
authors.forename: F
authors.initials: F
authors.lastname: Clostre
authors.forename: P
authors.initials: P
authors.lastname: Ladure
authors.forename: A
authors.initials: A
authors.lastname: Taccoen
mesh_terms: D002199:Capillary Permeability / Q000502:physiology; D002200:Capillary Resistance / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology; D008833:Microcirculation / Q000502:physiology*; D010972:Platelet Activating Factor / Q000502:physiology; D012212:Rheology; D014661:Vasoconstriction / Q000502:physiology*; D014689:Venous Insufficiency / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D016207:Cytokines; D010972:Platelet Activating Factor
vernacular_title: Microcirculation et rhéologie.