OXIDIZED LDL-INDUCED MICROVASCULAR DYSFUNCTION - DEPENDENCE ON OXIDATION PROCEDURE
OXIDIZED LDL-INDUCED MICROVASCULAR DYSFUNCTION - DEPENDENCE ON OXIDATION PROCEDURE
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DOI：
10.1161/01.atv.15.12.2305
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发表时间：
1995-12-01
影响因子：
8.7
通讯作者：
GRANGER, DN
中科院分区：
文献类型：
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作者：
LIAO, LX;AW, TY;GRANGER, DN
已知Cu 2+氧化的人LDL可促进白细胞-内皮细胞粘附（LECA）和毛细血管后微静脉中的白蛋白渗漏。本研究的目的是比较Cu ~（2+）氧化LDL（Cu-LDL）、磷脂酶A（2）加脂氧合酶（PLA（2）-LDL）、辣根过氧化物酶加过氧化氢（HRP-LDL）或-OCl氧化LDL（-OCl-LDL）促进（1）中性粒细胞-内皮细胞粘附（NECA）和（2）大鼠肠系膜微静脉LECA和白蛋白渗漏的能力。体外粘附试验表明，只有Cu-LDL引起剂量依赖性NECA反应，而PLA（2）-LDL（但非正常（N-LDL）、HRP-LDL或-OCl-LDL）在研究的最高浓度（670 μ g/mL）下增加NECA。不同形式的氧化LDL引起的NECA反应的幅度与脂质过氧化的程度有关，但与蛋白质氧化的水平无关。局部动脉灌注Cu-LDL、PLA（2）-LDL或-OCl-LDL可引起大鼠肠系膜微静脉白细胞粘附和游走、肥大细胞脱颗粒和白蛋白渗漏显著增加，但N-LDL无此作用。所有形式的氧化LDL诱导的LECA均未伴随微静脉剪切率的显著改变。
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 A(2) plus lipoxygenase (PLA(2)-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 PLA(2)-LDL but not normal (N-LDL), HRP-LDL, or -OCl-LDL increased NECA at the highest concentration studied (670 mu g/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, PLA(2)-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.