Kagan H M, Milbury P E, Kramsch D M
Circ Res. 1979 Jan;44(1):95-103. doi: 10.1161/01.res.44.1.95.
Thoracic aortae of normal rabbits were perfused with pancreatic elastase in vitro at 37 degrees C and 70 mm Hg pressure in the presence or absence of elastin ligands previously shown to stimulate or inhibit the enzymatic degradation of elastin. Perfusion with elastase results in an average of 3.6 lamellae degraded, whereas addition of sodium linoleate before and during the perfusion with elastase increases this value to 7.9 (P less than 0.001). Conversely, perfusion with the cationic detergent, dodecyltrimethylammonium chloride, completely prevents the degradation of elastic lamellae by elastase. These effects do not reflect alterations of the intrinsic catalytic activity of elastase, but apparently indicate the formation of complexes between the elastin ligands and arterial elastic lamellae, as is consistent with prior studies indicating such interactions between fatty acids or detergents and purified elastin. These studies suggest that agents such as fatty acids may significantly alter the metabolic susceptibility of elastin in vivo and possibly contribute to the degradation of elastic lamellae seen in arteries with advanced atherosclerosis.
在37摄氏度、70毫米汞柱压力下,于体外对正常兔的胸主动脉进行灌注,灌注液为胰弹性蛋白酶,同时存在或不存在先前已证明能刺激或抑制弹性蛋白酶解的弹性蛋白配体。用弹性蛋白酶灌注平均导致3.6层弹力膜降解,而在弹性蛋白酶灌注前及灌注过程中添加亚油酸钠可使该值增加至7.9(P<0.001)。相反,用阳离子去污剂十二烷基三甲基氯化铵灌注可完全阻止弹性蛋白酶对弹性膜的降解。这些效应并非反映弹性蛋白酶内在催化活性的改变,而是明显表明弹性蛋白配体与动脉弹性膜之间形成了复合物,这与先前关于脂肪酸或去污剂与纯化弹性蛋白之间存在此类相互作用的研究一致。这些研究表明,脂肪酸等物质可能会显著改变体内弹性蛋白的代谢敏感性,并可能导致在晚期动脉粥样硬化动脉中所见的弹性膜降解。