大鼠动脉粥样硬化模型的建立方法

目的:建立一种大鼠动脉粥样硬化模型的实验方法.方法:30只雌性SD大鼠随机分成正常对照组(C组,n=10)与模型组(M组,n=20只),C组普通饲料喂养,M组采用分次大剂量维生素D.注射 高脂饲料喂养,2个月后处死大鼠,检测血脂学变化,制作动脉切片进行形态学观察.结果:M组中的胆固醇、甘油三脂及低密度脂蛋白较C组显著升高(P＜0.01),高密度脂蛋白则较C组下降(P＜0.05).光镜下M组中膜严重钙化,明显不规则增厚,有泡沫细胞形成,平滑肌纤维排列显著紊乱等;C组主动脉平滑肌排列整齐规则,管腔内皮光滑,无增生.电镜下M组胶原纤维明显增多,排列紊乱,局灶性纤维溶解变性.局部有脂质样颗粒沉积在细胞间隙中.平滑肌细胞核固缩,核染色变深,部分可见坏死的平滑肌细胞,平滑肌细胞线粒体空泡化.内皮细胞大部分脱落,局灶有血栓形成(大量红细胞),可见有泡沫细胞.C组内皮完整,平滑肌纤维正常,排列紧密,胶原纤维排列规则,无增生.结论:用高脂饲料及大剂量维生素D.可有效诱发大鼠动脉粥样硬化.

Method of establishment of model of experimental atherosclerosis in rats

Objective:To establish an experimental method for atherosclerosis model of rats. Methods:Thirty Sprague-Dawley rats were divided into two groups randomly: control group(n=10) and model group(n=20).Control group fed with normal food, Model group fed with high cholesterol diet(1% cholesterol; 0.5% sodium cholate; 0.1% methimazole;5%lard) after intraperitoneal vitamin D3 (700,000 IU/kg, commonly four times at interval of two days) injection. Serum lipid and morphological change of aorta were determined after 2 months. Results: The levels of serum total cholesterol, low density lipoprotein (LDL) and triglyceride (TG) in model group were significantly higher than those in control group (P<0.01). The levels of high density lipoprotein(HDL) were obviously lower than those in control group(P<0.05). Compared with control group. There were serious calcification,irregularly thickening, disorganized fibers of vascular smooth muscle and some deposited foam cells in the tunica media of aorta under light microscope in the control group. Marked increase of disordered collagen local fiberous lysis and degeneration could be seen under electron microscope. Some lipid particles deposited among extracellular space, pycnosised and heavily stained nuclei of vascular smooth cells that even necrosed somewhere and vacuolated mitochondrions in some of them could be observed. Endothelial cell shedding, thrombosis and foam cell formation could also be observed. Conclusion: Rat can be used as a ideal model for research of atherosclerosis created by high cholesterol diet plus vitamin D3 overload.