Systemic vascular leakage

Resiniferatoxin-induced systemic vascular leakage (SYVAL). 

Another effect of disease states such as diabetes and proliferative diabetic retinopathy is an increase in the vitreous protein concentration, which may be partly, but not entirely, due to vascular leakage (102,103). Thus, the decreased permeability barrier (systemic to vitreous) and increased potential for protein binding within the vitreous will tend to increase vitreous drug concentrations. The increased intravitreal drug concentration is opposed by the decreased permeability barrier (vitreous to serum) that may enhance vitreous elimination. The process is further complicated by the effects of ocular diseases on active transport mechanisms. 

Anaphylaxis is the most dramatic and potentially catastrophic manifestation of allergic disorders. It can affect virtually any organ including the cardiovascular system. Cardiovascular collapse and hypotensive shock in anaphylaxis have been attributed to peripheral vasodilation, enhanced vascular permeability and plasma leakage, rather than any direct effect on the myocardium. However, there is increasing experimental and clinical evidence that the human heart is a site and target of anaphylaxis. 

Virus replicates in target organs such as local lymph nodes and liver, then released as a viremia, infecting WBC and lymphatic system and increasing vascular permeability causing massive fluid leakage... 

The marked injury to the epithelium is associated with severe abnormalities in surfactant function that were suspected when ARDS was originally described (9-11). Surfactant dysfunction is a consequence of severe injury to type II pneu-mocytes and inactivation of surfactant by plasma proteins leaking into the alveolar spaces from the vascular compartment. In addition, surfactant-associated proteins are reduced in the airspaces and appear in the systemic circulation, possibly by leakage out of the airspaces into the plasma (12,13). 

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