Mechanism of endothelial dysfunction in apolipoprotein E-deficient mice
Mechanism of endothelial dysfunction in apolipoprotein E-deficient mice
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DOI：
10.1161/01.atv.21.6.1017
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发表时间：
2001-06-01
影响因子：
8.7
通讯作者：
Katusic, ZS
中科院分区：
文献类型：
--
作者：
d'Uscio, LV;Baker, TA;Katusic, ZS
NO介导的内皮依赖性舒张功能在人类动脉粥样硬化小鼠模型中受损，我们的目的是描述载脂蛋白E（apoE）缺陷小鼠动脉粥样硬化中内皮功能障碍的机制，用富含脂质的西式饮食治疗26至29周。apoE缺陷小鼠的主动脉环对乙酰胆碱（10（-9）至10（-5）mol/L）和Ca 2+离子载体（10（-9）至10（-6）mol/L）的内皮依赖性舒张功能受损，对二乙基铵（Z）-1 -（N，N-二乙基氨基）二氮烯-1-鎓-1，2-二醇盐（DEA-NONOate，10（-10）to 10（-5）mol/L）与C57 BL/6 J小鼠主动脉环比较（P
Endothelium-dependent relaxations mediated by NO are impaired in a mouse model of human atherosclerosis, Our objective was to characterize the mechanisms underlying endothelial dysfunction in aortas of apolipoprotein E (apoE)-deficient mice, treated for 26 to 29 weeks with a lipid-rich Western-type diet. Aortic rings from apoE-deficient mice showed impaired endothelium-dependent relaxations to acetylcholine (10(-9) to 10(-5) mol/L) and Ca2+ ionophore (10(-9) to 10(-6) mol/L) and endothelium-independent relaxations to diethylammonium (Z)-1 -(N,N-diethylamino)diazen-1-ium-1,2-diolate (DEA-NONOate, 10(-10) to 10(-5) mol/L) compared with aortic rings from C57BL/6J mice (P