Johnson W T, Salanga G, Lee W, Marshall G A, Himelstein A L, Wall S J, Horwitz O
Atherosclerosis. 1986 Feb;59(2):161-71. doi: 10.1016/0021-9150(86)90045-6.
Sections of aorta, coronary artery, basilar artery and vena cava were collected at autopsy. Macroscopically normal intimal specimens were removed by stripping. Intimal collagen was measured as hydroxyproline. Intimal film embrittlement was measured in vitro by a bursting volume distensibility test developed in our laboratory. There was an average increase of over 100% in the collagen content of apparently lesion-free human arterial intima on aging over a fifty-year period. This includes an increase of 113% for aortic intima, 49% increase for coronary artery intima, and an increase of 158% in collagen in basilar artery intima. In contrast the collagen level in the vena caval intima decreases on aging, by 42% in fifty years. The large increase in collagen in arterial intima is accompanied by a large increase in intimal embrittlement. The decreasing collagen content of the venous intima on aging results in increased distensibility. Increased aortic intimal film embrittlement (lower distensibility) correlates with age (R = 0.699), but even better with intimal collagen (R = 0.911), suggesting that aortic intimal collagen level is a more important determinant of intimal embrittlement than age. Men, older than 55, have significantly higher aortic intimal collagen levels than women. Embrittlement of arterial intima should make it more susceptible to injury under the pulsatile pressure of the blood. Decreased venous intimal collagen and greater distensibility on aging could be factors in the development of venous valvular insufficiency and varicose veins. However, our study of veins was performed primarily as a control in this instance. Fundamental elements in the atherogenic process are increased intimal collagen, increased intimal brittleness, endothelial injury, followed by intimal cell proliferation. In the vena caval intima on aging there is decreased collagen, increased intimal distensibility, no injury due to increased pulse or blood pressure, and, therefore, no cell proliferation and no intimal lesion.
在尸检时采集主动脉、冠状动脉、基底动脉和腔静脉的切片。通过剥离获取宏观上正常的内膜标本。内膜胶原蛋白以羟脯氨酸进行测量。内膜膜脆性通过我们实验室开发的破裂容积扩张性试验在体外进行测量。在五十年的衰老过程中，看似无病变的人体动脉内膜的胶原蛋白含量平均增加超过100%。这包括主动脉内膜增加113%，冠状动脉内膜增加49%，基底动脉内膜胶原蛋白增加158%。相比之下，腔静脉内膜的胶原蛋白水平在衰老过程中下降，五十年内下降了42%。动脉内膜胶原蛋白的大幅增加伴随着内膜脆性的大幅增加。静脉内膜胶原蛋白含量随衰老而减少导致扩张性增加。主动脉内膜膜脆性增加（扩张性降低）与年龄相关（R = 0.699），但与内膜胶原蛋白的相关性更好（R = 0.911），这表明主动脉内膜胶原蛋白水平比年龄更重要地决定内膜脆性。55岁以上的男性主动脉内膜胶原蛋白水平明显高于女性。动脉内膜脆性增加应使其在血液的脉动压力下更容易受到损伤。静脉内膜胶原蛋白减少以及衰老时扩张性增加可能是静脉瓣膜功能不全和静脉曲张发展的因素。然而，在这种情况下，我们对静脉的研究主要是作为对照进行的。动脉粥样硬化形成过程中的基本要素是内膜胶原蛋白增加、内膜脆性增加、内皮损伤，随后是内膜细胞增殖。在腔静脉内膜衰老过程中，胶原蛋白减少，内膜扩张性增加，没有因脉搏或血压增加而导致的损伤，因此没有细胞增殖和内膜病变。
