Abstract
Objective: This review evaluates (1) the regulation of water and solute transport across the endothelial barrier in terms of pore theory and the glycocalyx-junction-break model of capillary permeability; and (2) the mechanisms regulating permeability based on experiments using cultured endothelial cells and intact microvessels.
Conclusions: The current form of the glycocalyx-junction-break model of capillary permeability describes the selectivity of the capillary wall (pore size) in terms of the space between the fibers of a quasi-periodic matrix on the endothelial cell surface, and the area for exchange (pore number) in terms of the length and frequency of breaks in the tight junction strands. An independent test of this model in a range of mammalian microvascular beds is new experimental evidence that the colloid osmotic pressure of plasma proteins is developed across the glycocalyx, not across the whole microvessel wall. We are beginning to understand that endothelial cells may change their phenotype in response to physical and chemical stresses. Such changes in phenotype may explain changes in the regulation of endothelial barrier function in intact microvessels that have previously been exposed to injury and differences in the regulation of contractile mechanisms between endothelial cells in vivo and in vitro.
