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用食饵性动脉粥样硬化（ＡＳ）模型，研究噻氯匹定的抗ＡＳ作用。噻氯匹定２０和６０ｍｇ·ｋｇ－１·ｄ－１连续８ｗｋ，ｐｏ，能显著抑制鹌鹑动脉内膜ＡＳ斑块形成．每２ｗｋ测定血清血脂，该药对甘油三酯，总胆固醇和低密度脂蛋白胆固醇水平无明显影响，但使高密度脂蛋白胆固醇略有升高．于ＡＳ造型２和４ｗｋ，血清ＮＯ水平下降；在ＡＳ造型６ｗｋ，ＮＯ水平升高，噻氯匹定可逆转ＡＳ造型引起的ＮＯ水平变化．用放免法分析该药对前列环素合成的影响，结果噻氯匹定３．３，１０和３０ｍｇ·ｋｇ－１，２４ｈ内ｉｇ３次，均显著提高大鼠动脉壁６－酮－前列腺素Ｆ１α含量．结果表明噻氯匹定可抑制鹌鹑实验性ＡＳ斑块形成，除抑制血小板功能外，保护内皮功能可能也是该药抑制ＡＳ病变形成的重要机理．
The anti-AS effect of ticlopidine was studied using an alimentary atherosclerosis (AS) model. Ticlopidine 20 and 60mg · kg-1 · d-1 for 8wk, po, can significantly inhibit quail artery intimal AS plaque formation. Serum lipids were measured every 2 weeks and had no significant effect on triglycerides, total cholesterol and LDL-C but slightly elevated HDL cholesterol. Serum NO levels decreased at 2 and 4 weeks after AS modeling. At the 6th week of AS modeling, the level of NO increased. Ticlopidine reversed the change of NO level caused by AS modeling. Using radioimmunoassay analysis of the drug on the synthesis of prostacyclin, results ticlopidine 3.3, 10 and 30mg · kg-1,24h ig 3 times, were significantly increased in rat arterial wall 6-keto-prostaglandin F1α content. The results show that ticlopidine can inhibit quail experimental AS plaque formation, in addition to inhibiting platelet function, the protection of endothelial function may also be an important mechanism of the drug to inhibit the formation of AS lesions.