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

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