Is there evidence for venular large junctional gap formation in inflammation?

Inflammatory edema is associated with vascular macromolecular leakage. Various patterns of vascular macromolecular leakage may be produced depending on the severity and nature of the inflammatory stimulus resulting in transient and/or sustained increases in macromolecular permeability. Inflammatory stimuli which cause endothelial cell damage or destruction induces non-specific increases in macromolecular permeability in all injured microvessels. In the absence of endothelial cell injury, macromolecular permeability is increased in inflammation subsequent to the formation of inter-endothelial cell gaps in capillaries and venules. Various inflammatory mediators including histamine-type agents, immune complexes, and activated leukocytes induce venular large junctional gap formation. Individual, simultaneous, or sequential mediator effects could explain the various patterns of venular macromolecular leakage found in inflammation. The formation of endothelial cell junctional gaps in capillaries cannot be attributed to any known inflammatory mediator. The classical static small pore/large pore model of the microvascular membrane cannot explain the increased extravasation of macromolecules in inflammation. A dual static/variable large pore system would best describe macromolecular transport under normal and inflammatory conditions.