Polymorphonuclear leukocyte-induced vasocontraction and endothelial dysfunction. Role of selectins.

摘要: The roles of selectin adhesion molecules (P- and L-selectin) their counterreceptor sialyl Lewisx were investigated in polymorphonuclear leukocyte (PMN)-induced cat coronary vasocontraction endothelial dysfunction. Unstimulated autologous PMNs (10(6) cells/mL) added to organ chambers containing artery rings stimulated with either thrombin (2 U/mL) or hydrogen peroxide (100 mumol/L). elicited a significant thrombin- (119 +/- 14 mg) peroxide- (132 15 rings. This PMN-induced was significantly attenuated by pretreatment an anti-P-selectin, anti-L-selectin monoclonal antibody (ie, MAb PB 1.3 DREG-200), Lewis(x)-containing oligosaccharide (SLe(x)-OS). Endothelial function as assessed endothelium-dependent vasorelaxation acetylcholine also after dysfunction prevented 1.3, DREG-200, SLe(x)-OS. In contrast, endothelium-independent relaxation acidified sodium nitrite not altered PMN incubation, indicating that vascular smooth muscle unaffected. Adherence endothelium increased following stimulation peroxide, but this Thus, PMN-endothelial interaction mediated P-selectin Lewis(x) may play important role mechanism be the early observed reperfusion ischemic vasculature.