Interendothelial junctions of the rabbit iris vasculature in anterior uveitis.

Ultrastructural tracer techniques and freeze-fracture electron microscopy were used to evaluate the alterations present in the tight junctions of rabbit iris blood vessels in anterior uveitis. In control animals, the iris vascular endothelial cells were seen to be joined by both tight and gap junctions. Leakage of tracer from these vessels was not observed. Freeze-fracture replicas of the tight junctions in these vessels revealed two to eight branching and anastomosing strands, the particles of which tended to remain with the E fracture face. Experimental animals received intravitreal injections of 1.0 microgram of E. coli endotoxin. Twenty-four hours later, at peak severity of the inflammatory response, the animals were sacrificed. Iris vessels from uveitic eyes were observed to leak tracer, primarily through their interendothelial clefts. In freeze-fracture replicas, junctional changes took two major forms. In most cases, junctional simplification was observed. Only one or two continuous strands were evident, with very few interstrand anastomoses. In fewer instances, focal areas of profound junctional disruption were seen. In the latter case, short strands of tight junctional particles remained but the complementary ridge and groove system characteristic of tight junctions was lost. The loss of this system is interpreted to indicate that separation of adjacent endothelial cells, and an opening of the interendothelial cell cleft, has occurred at these locations. Both junctional simplification and junctional disruption likely result in increased vascular permeability. It is not possible to judge the relative contributions to increased vascular permeability which attend widespread junctional simplification as opposed to rare, focal junctional disruptions.(ABSTRACT TRUNCATED AT 250 WORDS)