Miwa K, Miyagi Y, Fujita M
Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
J Am Coll Cardiol. 1995 Sep;26(3):632-8. doi: 10.1016/0735-1097(95)00207-K.
The purpose of this study was to investigate the peroxidative susceptibility of plasma low density lipoprotein in patients with active variant angina and to compare it with that in subjects without coronary spasm.
Oxidized or modified low density lipoprotein can impair endothelium-dependent vasoregulation and has atherogenic properties; it may be related to the genesis of coronary artery spasm by potentiating agonist-induced vasoconstriction.
The sensitivity of plasma low density lipoprotein for cupric ion (Cu2+)-induced peroxidation was examined. Low density lipoprotein was isolated from plasma in 112 patients: 21 with active variant angina, 18 with inactive variant angina without anginal attacks during the preceding 6 months, 39 with significant organic coronary artery stenoses but without rest angina and 34 control subjects without coronary artery disease. Lipid peroxidation products in low density lipoprotein were assayed as thiobarbituric acid-reactive substances before and after incubation with various concentrations of Cu2+ at 37 degrees C for 24 h.
Significantly higher levels of generation of thiobarbituric acid-reactive substances from plasma low density lipoprotein after incubation with Cu2+ were seen in patients with active variant angina than in patients in the other three groups. The dose-response curve of low density lipoprotein peroxidation induced by Cu2+ shifted to the left in this group as compared with the curve in the other three groups. The vitamin E (alphatocopherol) content of low density lipoprotein fraction in these patients was significantly lower than that in the other groups. After > or = 6 months of an angina-free period in five patients with active variant angina, thiobarbituric acid-reactive substances induced by 0.5 mumol/liter Cu2+ in low density lipoprotein were significantly decreased and vitamin E content was significantly increased.
These results indicate that vitamin E-deficient plasma low density lipoprotein in patients with active variant angina is highly susceptible to peroxidative modification.
本研究旨在调查活动型变异型心绞痛患者血浆低密度脂蛋白的过氧化易感性，并将其与无冠状动脉痉挛的受试者进行比较。
氧化或修饰的低密度脂蛋白可损害内皮依赖性血管调节并具有致动脉粥样硬化特性；它可能通过增强激动剂诱导的血管收缩与冠状动脉痉挛的发生有关。
检测血浆低密度脂蛋白对铜离子（Cu2+）诱导的过氧化作用的敏感性。从112例患者的血浆中分离出低密度脂蛋白：21例活动型变异型心绞痛患者，18例非活动型变异型心绞痛患者（前6个月无心绞痛发作），39例有明显器质性冠状动脉狭窄但无静息性心绞痛患者以及３4例无冠状动脉疾病的对照受试者。在37℃下将低密度脂蛋白与不同浓度的Cu2+孵育24小时前后，将低密度脂蛋白中的脂质过氧化产物测定为硫代巴比妥酸反应性物质。
与其他三组患者相比，活动型变异型心绞痛患者在与Cu2+孵育后，血浆低密度脂蛋白产生的硫代巴比妥酸反应性物质水平显著更高。与其他三组曲线相比，该组中Cu2+诱导的低密度脂蛋白过氧化的剂量反应曲线向左移动。这些患者低密度脂蛋白组分中的维生素E（α-生育酚）含量明显低于其他组。五例活动型变异型心绞痛患者在无心绞痛期≥6个月后，0.5μmol /升Cu2+诱导的低密度脂蛋白中的硫代巴比妥酸反应性物质显著降低，维生素E含量显著增加。
这些结果表明，活动型变异型心绞痛患者中维生素E缺乏的血浆低密度脂蛋白极易发生过氧化修饰。
