Lindén T, Camejo G, Wiklund O, Warnold I, Olofsson S O, Bondjers G
Wallenberg Laboratory for Cardiovascular Research, Department of Medicine I, Gothenburg University, Sahlgrenska Hospital, Sweden.
J Clin Pharmacol. 1990 Feb;30(S2):S124-31. doi: 10.1002/j.1552-4604.1990.tb03510.x.
In view of conflicting evidence suggesting that beta-blockers have an anti-atherogenic effect as well as induce a potentially atherogenic lipoprotein profile, the effects of a short term beta-blockade on serum lipoproteins were studied in 39 healthy volunteers. Because the interaction of LDL with arterial proteoglycans appears to play a role in lipoprotein accumulation during atherogenesis, the effects of metoprolol and atenolol on low density lipoprotein interaction with human aortic proteoglycans were included in the study. We could confirm that the beta-blockers caused a decrease in HDL cholesterol and an increase in triglycerides, both potentially undesirable effects. In addition, however they induced a significant decrease in the in vitro LDL affinity for arterial proteoglycans. Since there appears to be a strong association between LDL reactivity with proteoglycans and risk for myocardial infarction, this effect of the beta-blockers may be an anti-atherogenic effect which overrides other effects on the lipoprotein pattern.
鉴于有相互矛盾的证据表明β受体阻滞剂具有抗动脉粥样硬化作用，同时也会导致潜在的致动脉粥样硬化脂蛋白谱，我们对39名健康志愿者进行了短期β受体阻滞剂治疗对血清脂蛋白影响的研究。由于低密度脂蛋白（LDL）与动脉蛋白聚糖的相互作用似乎在动脉粥样硬化形成过程中的脂蛋白积聚中起作用，因此美托洛尔和阿替洛尔对低密度脂蛋白与人主动脉蛋白聚糖相互作用的影响也纳入了本研究。我们可以证实，β受体阻滞剂导致高密度脂蛋白胆固醇降低和甘油三酯升高，这两种都是潜在的不良影响。然而，除此之外，它们还导致体外LDL对动脉蛋白聚糖的亲和力显著降低。由于LDL与蛋白聚糖的反应性与心肌梗死风险之间似乎存在密切关联，β受体阻滞剂的这种作用可能是一种抗动脉粥样硬化作用，它超过了对脂蛋白模式的其他影响。
