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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1995;15:2305-2311.)
© 1995 American Heart Association, Inc.

Articles

Oxidized LDL–Induced Microvascular Dysfunction

Dependence on Oxidation Procedure

Lianxi Liao; Tak Yee Aw; Peter R. Kvietys; D. Neil Granger

From the Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport.

Correspondence to Dr D. Neil Granger, Department of Physiology and Biophysics, LSU Medical Center, 1501 Kings Hwy, PO Box 33932, Shreveport, LA 71130-3932.

Abstract Human LDLs oxidized with Cu²⁺ are known to promote leukocyte–endothelial cell adhesion (LECA) and albumin leakage in postcapillary venules. The objective of this study was to compare the ability of LDL oxidized with Cu²⁺ (Cu-LDL), phospholipase A₂ plus lipoxygenase (PLA₂-LDL), horseradish peroxidase plus H₂O₂ (HRP-LDL), or -OCl (-OCl-LDL) to promote (1)neutrophil–endothelial cell adhesion (NECA) in vitro and (2)LECA and albumin leakage in rat mesenteric venules. In vitro adhesion assays revealed that only Cu-LDL elicited a dose-dependent NECA response, whereas PLA₂-LDL but not normal (N-LDL), HRP-LDL, or -OCl-LDL increased NECA at the highest concentration studied (670 µg/mL). The magnitude of the NECA responses elicited by the different forms of oxidized LDL was related to the degree of lipid peroxidation but unrelated to the level of protein oxidation. Local intra-arterial infusion of Cu-LDL, PLA₂-LDL, or -OCl-LDL but not N-LDL elicited significant increases in leukocyte adherence and emigration, mast cell degranulation, and albumin leakage in rat mesenteric venules. The LECA induced by all forms of oxidized LDL was not accompanied by significant alterations of venular shear rate.

Key Words: lipoproteins, low-density • adhesion, leukocyte–endothelial cell • permeability, vascular • degranulation, mast cell • oxidation

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