H Vink1, A A Constantinescu, J A Spaan. 1. Department of Medical Physics, University of Amsterdam, Amsterdam, The Netherlands. h.vink@amc.uva.nl
Abstract
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.
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.
Authors: Sarah L Waters; Jordi Alastruey; Daniel A Beard; Peter H M Bovendeerd; Peter F Davies; Girija Jayaraman; Oliver E Jensen; Jack Lee; Kim H Parker; Aleksander S Popel; Timothy W Secomb; Maria Siebes; Spencer J Sherwin; Rebecca J Shipley; Nicolas P Smith; Frans N van de Vosse Journal: Prog Biophys Mol Biol Date: 2010-10-30 Impact factor: 3.667
Authors: Sietze Reitsma; Dick W Slaaf; Hans Vink; Marc A M J van Zandvoort; Mirjam G A oude Egbrink Journal: Pflugers Arch Date: 2007-01-26 Impact factor: 3.657
Authors: Daniel R Machin; Samuel I Bloom; Robert A Campbell; Tam T T Phuong; Phillip E Gates; Lisa A Lesniewski; Matthew T Rondina; Anthony J Donato Journal: Am J Physiol Heart Circ Physiol Date: 2018-05-11 Impact factor: 4.733
Authors: Jurgen W G E VanTeeffelen; Alina A Constantinescu; Judith Brands; Jos A E Spaan; Hans Vink Journal: J Physiol Date: 2008-05-01 Impact factor: 5.182