Born G V, Medina R, Shafi S, Cardona-Sanclemente L E
William Harvey Research Institute, University of London.
C R Seances Soc Biol Fil. 1998;192(5):947-61.
Our experiments were done to find out whether there are factors which influence the passage of the two major "risk factor proteins" LDL and fibrinogen, other than their plasma concentrations, from the blood into the arterial walls, where their accumulation is associated with atherogenesis. The results suggest that administration of a remarkable variety of pressor agents over a few days accelerate the uptake of both proteins by arterial walls, and that, in contrast, the process is no faster in rats that have been spontaneously, i.e., genetically, hypertensive for about 3 months. Considering our experimental findings in relation to human atherosclerotic disease, it is interesting that the risk of coronary heart disease and stroke is increased more than additively when both LDL or fibrinogen levels and systolic or diastolic blood pressures are high (18,46). If our work should point to some mechanistic connection between blood pressure and the accumulation of atherogenic plasma proteins in arterial walls, it would provide, at least in principle, an explanation for the epidemiological facts.
我们开展这些实验是为了找出,除了血浆浓度之外,是否存在影响两种主要“风险因子蛋白”——低密度脂蛋白(LDL)和纤维蛋白原——从血液进入动脉壁的因素,而它们在动脉壁中的积聚与动脉粥样硬化的发生有关。结果表明,在几天内给予多种不同的升压药会加速动脉壁对这两种蛋白的摄取,相反,对于已经自发(即遗传性)高血压约3个月的大鼠,这个过程并没有加快。结合我们关于人类动脉粥样硬化疾病的实验结果来看,有意思的是,当低密度脂蛋白或纤维蛋白原水平以及收缩压或舒张压都很高时,冠心病和中风的风险增加幅度超过两者单独作用的叠加(18,46)。如果我们的研究能够指出血压与动脉壁中致动脉粥样硬化血浆蛋白积聚之间的某种机制联系,那么至少在理论上,它将为这些流行病学事实提供一种解释。