PHYSICOCHEMICAL AND HISTOLOGICAL-CHANGES IN THE ARTERIAL-WALL OF NONHUMAN-PRIMATES DURING PROGRESSION AND REGRESSION OF ATHEROSCLEROSIS
PHYSICOCHEMICAL AND HISTOLOGICAL-CHANGES IN THE ARTERIAL-WALL OF NONHUMAN-PRIMATES DURING PROGRESSION AND REGRESSION OF ATHEROSCLEROSIS
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DOI：
10.1172/jci111366
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发表时间：
1984-01-01
影响因子：
15.9
通讯作者：
SAWYER, JK
中科院分区：
文献类型：
--
作者：
SMALL, DM;BOND, MG;SAWYER, JK
为了确定非人灵长类动物动脉粥样硬化进展和消退过程中发生的时间变化，在饮食诱导的高胆固醇血症30分钟进展期和12个月期间研究了动脉壁病变的理化和组织学特征。回归时期。研究了三组猕猴（Macaca fascicularis）。对照组饲喂基础日粮，进展组饲喂高胆固醇日粮。回归组喂食高胆固醇饲料18个月，然后喂食猴子食物长达12个月。对照动物的胆固醇酯很少，泡沫细胞很少，没有细胞外胆固醇酯滴或胆固醇晶体。在进展过程中，最初含有高熔点细胞内胆固醇酯滴的泡沫细胞数量增加。到30个月时，胆固醇结晶和坏死占主导地位，高熔融泡沫细胞仅出现在病变边缘，表明初始过程在病变边缘继续。细胞外酯的熔点较低表明其脂质组成不同于细胞内滴。在这些动物中观察到的变化通常反映了对人类动脉粥样硬化进展的预测。在退化的最初6mo，坏死仍然存在，泡沫细胞数量减少，胆固醇酯含量降低；但游离胆固醇含量的相对比例增加，形成大量的胆固醇结晶。因此，血清胆固醇浓度的大幅和快速下降实际上可能导致一水胆固醇的沉淀和病变的明显恶化。更长时间的消退（12个月）倾向于使动脉壁的脂质成分恢复正常，部分减少胆固醇结晶，并导致内膜改善但结疤。
To identify the temporal changes occurring during progression and regression of atherosclerosis in nonhuman primates, the physiochemical and histological characteristics of arterial wall lesions were studied during a 30-min progression period of diet-induced hypercholesterolemia and during a 12-mo. period of regression. Three groups of cynomolgous monkeys (Macaca fascicularis) were studied. Control groups were fed a basal chow diet and progression groups were fed a high-cholesterol-containing diet. Regression groups were fed a high-cholesterol diet for 18 mo. and then fed monkey chow for up to 12 mo. Control animals had very little cholesterol ester, rare foam cells, and no extracellular cholesterol ester droplets or cholesterol crystals. During progression there is initially an increase in the number of foam cells containing very high-melting intracellular cholesterol ester droplets. By 30 mo., cholesterol crystals and necrosis dominate and high-melting foam cells appear only at lesion margins, suggesting that the initial process continues at the lesion edge. The lower melting point of extracellular esters indicates a lipid composition different from intracellular droplets. The changes observed in these animals generally reflect those predicted for progression of human atherosclerosis. During the initial 6 mo. of regression, necrosis remains, the number of foam cells decreases, and cholesterol ester content decreases; however the relative proportion of free cholesterol content increases, and large numbers of cholesterol crystals are formed. Thus, large and rapid decreases in serum cholesterol concentration to produce regression in fact may result in the precipitation of cholesterol monohydrate and an apparent worsening of the lesions. More prolonged regression (12-mo.) tends to return the lipid composition of the artery wall towards normal, partially reduces cholesterol crystals, and results in an improved but scarred intima.