Albumin transfer across endothelial monolayers

Recently, Shasby and co-workers demonstrated increased albumin transfer across endothelial monolayers when human granulocytes and arachidonic acid were applied in combination but not when arachidonic acid was applied alone, indicating that, in neutrophils, arachidonic acid had acted as a substrate in the metabolic production of a substance with permeability enhancing properties, or had unmasked an oedematogenic property of neutrophils. 

The mechanism of action and the injury potential of lipid mediators are still a matter of debate (Figure 4.3). Malik and co-workers recently reviewed the role of cellular and humoral mediators in pulmonary oedema and concluded that few humoral factors act independently to increase capillary permeability and that these mediators might cause pulmonary venoconstriction and raise pulmonary capillary hydrostatic pressure. This concept is in agreement with results of Shasby et al which demonstrated that leukotriene C4 applied directly to an endothelium monolayer did not accelerate albumin transfer across the monolayer. However, because the culture medium was rich in serum proteins (which avidly bind leukotrienes ), one cannot rule out a direct damaging effect to endothelial cells given access of the molecule to the endothelial cell. 

Hennig, B., Enoch, C. and Chow, C.K. (1986) Linoleic acid hydroperoxide increases the transfer of albumin across cultured endothelial monolayers. Arch. Biochem. Biophys. 248, 353-357. 

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