Modulation of cultured pulmonary microvessel and arterial endothelial cell barrier structure and function by serotonin.

摘要: Abstract Pulmonary microvessel endothelial cell and pulmonary artery monolayers in tissue culture were treated with serotonin (5-hydroxytryptamine; 5-HT) alone or conjunction histamine, bradykinin, the thromboxane analog U-46619, actin modulating agent cytochalasin B. After treatment, cross-sections through (EC) examined by light microscopy percentage widths of intercellular openings quantitated. To correlate structural changes barrier an alteration permeability, EC cultured on micropore filters assayed for transit Evan's blue albumin (EBA) following treatment vasoactive mediators. 5-HT was found to decrease patency junctions up 94%, compared untreated monolayers, prevent reverse appearance interendothelial gaps induced The effect dose time dependent, a maximal increase junctional apposition observed at concentration 10 −6 M 30 min. This response significantly blocked antagonists LSD ketanserin. formation reduction U-46619 5-HT, respectively, positively correlated monolayer permeability EBA. These results suggest that edema caused inflammatory mediators part may be consequence transient increases gaps, contribute homeostatic maintenance integrity.