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目的:探讨氧化修饰低密度脂蛋白(Ox-LDL)对血管舒张的影响及高脂血症男性患者易患动脉粥样硬化(AS)的机制。方法:采用Cu2+对13例健康自愿者及29例高脂血症患者的低密度脂蛋白(LDL)进行氧化修饰,硫代巴比妥酸法测定丙二醛(MDA)含量,Bartlett法测定溶血卵磷脂(LPC)含量,乙酰胆碱诱发血管舒张。结果:健康人和高脂血症患者血浆LDL被氧化修饰后与修饰前比较MDA含量显著增高(P<0.01);两组Ox-LDL中的LPC水平均明显高于各自天然低密度脂蛋白(N-LDL)中的LPC水平(P<0.05);且健康人及高脂血症男性患者N-LDL中的LPC含量与女性基本相同,但两组男性Ox-LDL中的LPC含量高于女性(P<0.05),男性高脂血症患者Ox-LDL的LPC含量最高;两组Ox-LDL均明显抑制血管内皮依赖性舒张,与女性相比,健康男性Ox-LDL抑制血管舒张程度略强,但高脂血症男性患者Ox-LDL抑制血管舒张程度明显增强。高脂血症男性及女性患者Ox-LDL的抑制血管舒张效应与LPC量呈正相关(r=0.592,P<0.05;r=0.816,P<0.05)。结论:男性高脂血症患者易患AS可能与Ox-LDL增加LPC含量及抑制内皮依赖性血管舒张有关。
Objective: To investigate the effects of Ox-LDL on vasodilation and the mechanism of susceptibility to atherosclerosis (AS) in male patients with hyperlipidemia. Methods: LDL of 13 healthy volunteers and 29 patients with hyperlipidemia were oxidatively modified by Cu2 +, the malondialdehyde (MDA) content was measured by thiobarbituric acid method, and the hemolysis Lecithin (LPC) content, acetylcholine-induced vasodilation. Results: Compared with the pre-modification, the content of MDA in LDL was significantly increased (P <0.01) in both healthy subjects and patients with hyperlipidemia. The levels of LPC in both groups were significantly higher than those of native LDL (P <0.05). The content of LPC in N-LDL in healthy and hyperlipidemic men was similar to that in female, but the LPC content in Ox-LDL in both groups was higher than that in female (P <0.05). Ox-LDL in male patients with hyperlipemia had the highest LPC content. Ox-LDL in both groups significantly inhibited endothelium-dependent vasodilation. Ox-LDL inhibited vasodilatation slightly in healthy male , Ox-LDL in male patients with hyperlipidemia significantly inhibited vasodilation. Ox-LDL inhibition of vasodilatation in hyperlipidemic male and female patients was positively correlated with LPC volume (r = 0.592, P <0.05; r = 0.816, P <0.05). Conclusion: The predisposition of AS in male patients with hyperlipidemia may be related to the increase of LPC content and the inhibition of endothelium-dependent vasodilation by Ox-LDL.