Fluid exchange disorders due to capillary lesions are numerous and their extent depends on the underlying disease as well as the capillary structure of the affected organ. The inflammatory cascade, triggered by sepsis or reperfusion injury, is mediated by several humoral mediators and activated blood cells. These include pro-inflammatory cytokines, arachidonic acid, proteases, oxygen free radicals, polymorphonuclears, procoagulant, complement and fibrinolytic system. The interaction between 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 permeability induces transcapillary exudation of water and protein in the interstitial space, leading to organ dysfunction, mainly the lungs and splanchnic organs. Nitric oxyde, by modulating the response of the endothelium 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 oedema, and overinflation injury from mechanical ventilation. The anatomic specific features of the cerebral capillaries resulted in the well known concept of blood brain barrier with it's changeing morphology. Under the effect of humoral mediators and cellular interactions, the endothelial cells are able, via a calcium-mediated mechanism, to contract and to modify capillary permeability, leading to vasogenic oedema.