DISTURBANCES OF TRANSVASCULAR FLUID EXCHA NGES BY CAPILLARY INJURY

Fluid exchange disorders due to capillary lesions are numerous and the ir extent depends on the underlying disease as well as the capillary s tructure of the affected organ. The inflammatory cascade; triggered by sepsis or reperfusion injury, is mediated by several humoral mediator s and activated blood cells. These include pro-inflammatory cytokines, arachidonic acid, proteases, oxygen free radicals, polymorphonuclears , procoagulant, complement and fibrinolytic system. The interaction be tween these mediators leads to a loss of endothelial integrity, a loss of basment membrane and a disruption of the interstitial matrix, with wasting of the endothelial cytoskeleton. The alteration in permeabili ty induces transcapillary exudation of water and protein in the inters titial space, leading to organ dysfunction, mainly the lungs and splan chnic organs. Nitric oxyde, by modulating the response of the endothel ium to the cellular interaction may protect against capillary injury. Capillary ''stress lesions'' following microvascular hypertension are the physiological basis of neurogenic or high altitude pulmonary oedem a, and overinflation injury from mechanical ventilation. The anatomic specific features of the cerebral capillaries resulted in the well kno wn concept of blood brain barrier with iis changeing morphology. Under the effect of humoral mediators and cellular interactions, the endoth elial cells are able, via a calcium-mediated mechanism, to contract an d to modify capillary permeability, leading to vasogenic oedema.