PERMEABILITY-RELATED CHANGES REVEALED AT ENDOTHELIAL-CELL BORDERS IN INFLAMED VENULES BY LECTIN-BINDING

Plasma leakage in inflammation results from intercellular gaps that fo rm in the endothelium of venules. These gaps and related morphological changes in endothelial cells are not readily seen by light microscopy . In this study we sought to visualize such changes by using the selec tive binding properties of plant lectins. Acute inflammation was induc ed in the trachea of pathogen-free F344 rats by injecting substance P intravenously, and 1, 3, or 10 min later the vasculature was perfused with fixative followed by a biotinylated lectin. Lectin binding was lo calized by avidin-biotin complex-peroxidase histochemistry and viewed in tracheal whole mounts by differential-interference contrast microsc opy. The binding patterns of the 20 lectins tested fell into 4 groups. Most of the lectins either bound uniformly to the endothelium of norm al and inflamed venules (group 1, e.g., Lycopersicon esculentum lectin ) or bound weakly or not at all to venules (group 2, e.g., Maackia amu rensis I lectin). The uniform binding of group 1 lectins not only reve aled the overall vascular architecture but also made visible intercell ular gaps and fingerlike processes at endothelial cell borders in infl amed venules. In postcapillary venules after substance P, the fingerli ke processes were present along an average of 32% of the endothelial c ell perimeter at 1 min, 25% at 3 min, and 7% at 10 min, compared with a baseline value of 2%. A third group of lectins (group 3, e.g., conca navalin A) bound selectively to focal patches of inflamed venules but bound weakly to normal venules. The fourth group (group 4, e.g., Ricin us communis I lectin) bound preferentially to focal patches in inflame d venules and also bound uniformly to normal venules. The focal bindin g of group 3 and 4 lectins coincided with sites of plasma leakage mark ed by extravasation of the particulate tracer monastral blue and was a ssociated with subendothelial components of the vessel wall. We conclu de that selected lectins reveal novel features of focal sites of plasm a leakage, endothelial gaps, and fingerlike processes at endothelial c ell borders in inflamed venules.