Key result
Intravenous oxidized LDL reduces the endothelial surface layer ~60% and promotes platelet adhesion.
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BACKGROUND: Flowing erythrocytes and platelets are separated from the luminal endothelial cell (EC) surface by a 0.5-microm-wide space named the endothelial surface layer. We hypothesized that the disruption of the endothelial surface layer by oxidized low-density lipoproteins (Ox-LDL) contributes to atherogenic increases in vascular wall adhesiveness. METHODS AND RESULTS: The hamster cremaster muscle preparation was used for intravital microscopic observation of the distance between erythrocytes and the capillary EC surface. Moderate Ox-LDL was prepared by exposing native LDL to CuSO(4) for 6 hours. The dimension of the EC surface layer averaged 0.6+/-0.1 microm during control situations, but a bolus intravenous injection of Ox-LDL (0.4 mg/100 g of body weight) transiently diminished the EC surface layer by 60% within 25 minutes, which correlated with a transient increase in the number of platelet-EC adhesions. Combined administration of superoxide dismutase and catalase completely blocked the effect of Ox-LDL on the dimension of the EC surface layer and inhibited platelet-EC adhesion. CONCLUSIONS: Oxygen-derived free radicals mediate the disruption of the EC surface layer and increase vascular wall adhesiveness by Ox-LDL.
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Vink et al. (2000) studied Atherogenic vascular wall adhesiveness / endothelial surface layer disruption. Oxidized low-density lipoproteins (Ox-LDL) vs. Control situations and combined administration of superoxide dismutase and catalase was evaluated on Dimension of the endothelial cell surface layer (60% reduction). Intravenous oxidized LDL (0.4 mg/100 g) transiently diminished the endothelial surface layer by 60% from 0.6±0.1 µm within 25 minutes and increased platelet-endothelial adhesions.
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