您的位置：山东大学 -> 科技期刊社 -> 《山东大学学报（医学版）》

山东大学学报（医学版） ›› 2015, Vol. 53 ›› Issue (5): 10-14.doi: 10.6040/j.issn.1671-7554.0.2015.271

• 基础医学 • 上一篇    下一篇

血管内超声检测阿托伐他汀对兔动脉粥样硬化斑块的影响

谭蓓1, 关玉庆2, 孙慧2, 户克庆2, 苏国海2, 韦敏3   

  1. 1. 医学院, 山东 济南 250012;
    2. 附属济南市中心医院心内科, 山东 济南 250013;
    3. 附属济南市中心医院供应科, 山东 济南 250013
  • 收稿日期:2015-03-13 修回日期:2015-05-04 出版日期:2015-05-10 发布日期:2015-05-10
  • 通讯作者: 苏国海。E-mail:guohaisu@medmail.com.cn E-mail:guohaisu@medmail.com.cn
  • 基金资助:
    国家自然科学基金(81170087); 济南市企业自主创新计划(201003112)

Effects of atorvastatin with intravascular ultrasound on atherosclerotic plaques in rabbits

TAN Bei1, GUAN Yuqing2, SUN Hui2, HU Keqing2, SU Guohai2, WEI Min3   

  1. 1. School of Medicine, Jinan 250012, Shandong, China;
    2. Department of Cardiology;
    3. Department of Supplies, Jinan Central Hospital, Shandong University, Jinan 250013, Shandong, China
  • Received:2015-03-13 Revised:2015-05-04 Online:2015-05-10 Published:2015-05-10

PDF (PC)

131

摘要： 目的 采用血管内超声评价短期内不同剂量阿托伐他汀对动脉粥样硬化 (AS) 家兔模型斑块的影响。方法 30只新西兰大白兔随机分为对照组(n=7)、模型组(n=7)、阿托伐他汀低剂量组(n=8)和阿托伐他汀高剂量组(n=8)。对照组给予普通饲料喂养,其他各组均通过8周高脂喂养联合腹主动脉球囊损伤术建立AS模型。于第8周末行血管内超声检查。8周后,模型组,阿托伐他汀低、高剂量组继续高脂喂养,分别给予低、高剂量组兔不同剂量的阿托伐他汀干预2周。10周处死所有动物。抽取兔静脉血,测定血清血脂水平,应用ELISA法测定血清超敏C反应蛋白(hs-CRP)。并行血管内超声和病理组织学检查。结果 对照组血脂水平明显低于其他各组(P<0.05),阿托伐他汀低、高剂量两组血脂水平和血清hs-CRP水平明显低于模型组(P<0.05),且高剂量组变化更加明显(P<0.01)。血管内超声显示模型组的血管外弹力膜面积(EEMA)、斑块面积(PA)、管腔面积狭窄率(LAS%)明显大于低、高剂量组(P<0.05),管腔面积(LA)差异无统计学意义(P>0.05)。结论 阿托伐他汀能够短时间内降低AS兔的血脂水平,并减少AS兔斑块的形成,且与药物剂量呈正相关。

关键词: 阿托伐他汀, 血管内超声, 动脉粥样硬化, 兔, 斑块

Abstract: Objective To explore the effects of different doses of atorvastatin on atherosclerotic plaques in rabbit models with intravascular ultrasound. Methods A total of 30 New Zealand white rabbits were randomized into the control group (n=7), model group (n=7), low-dosage atorvastain group (n=8) and high-dosage atorvastain group (n=8). Except for the control group, the other groups were fed with high-fat diet for 8 weeks, and aortaventralis balloon-dilation injury was created to establish AS models. Intravascular ultrasound (IVUS) was performed at the end of the 8th week. After that, the model group continued to eat high-fat diet, while the two atorvastatin groups received 2-week extra atorvastatin intervention. At the end of the 10th week, all rabbits were sacrificed. Venous blood was drawn to measure serum lipid, and the amount of inflammation mediator hs-CRP was quantified with ELISA. The abdominal aortae were detected with IVUS and then observed pathologically. Results At the end of study, serum lipid in the control group was significantly lower than that in the other three groups (P<0.05). Compared with model group, the level of serum lipid and hs-CRP decreased significantly in two atorvastatin groups, which were more significant in high-dosage atorvastain group (P<0.01). Extra-elastic membranous area (EEMA), plaque area (PA), and lumen area stenosing (LAS%) in the model group were significantly higher than those in the two atorvastatin groups (P<0.05), with nosignificant difference in lumen area between the model group and the two atorvastatin groups (P>0.05). Conclusion Atorvastatin is able to control the level of serum lipid observably and reduce the plaque formation in atherosclerotic rabbit models.

Key words: Atorvastatin, Plaque, Intravascular ultrasound, Atherosclerosis, Rabbits

中图分类号: 

  • R541.4
[1] Cheng JM, Oemrawsingh RM, Garcia-Garcia HM, et al. Relation of C-reactive protein to coronary plaque characteristics on grayscale, radiofrequency intravascular ultrasound, and cardiovascular in patients with acute coronary syndrome or stable angina pectoris (from the ATHEROREMO-IVUS study)[J]. AM J Cardiol, 2014, 114(10): 1497-1503.
[2] Kwang K. Effects of statins on vascular wall: vasomotor function, inflammation, and plaque stability[J]. Cardio Res, 2000, 47(4): 648-657.
[3] 陈文强, 张立, 张梅. 血管内超声和病理学分析对比研究动脉粥样硬化兔不稳定斑块的破裂和血栓形成[J]. 中华超声和影像学杂志, 2004, 13(10): 777-779. CHEN Wenqiang, ZHANG Li, ZHANG Mei. Intravascular ultrasound versus pathologic analysis in detecting atherosclerotic plaque distruption and arterial thrombosis[J]. Chinese Journal of Ultarsonography, 2014, 13(10): 777-779.
[4] 仲琳, 张运, 张梅. 兔动脉粥样硬化易损斑块模型的建立[J]. 基础医学与临床, 2005, 25(4): 370-373. ZHONG Lin, ZHANG Yun, ZHANG Mei. An experimental study on vulnerable atherosclerotic plaques with intravascular ultrasound[J]. Basic and Clinical Medicine, 2005, 25(4): 370-373.
[5] 康卫平, 王萍, 王雪梅, 等. 兔腹主动脉粥样硬化模型的建立[J]. 临床医药实践杂志, 2007, 34(11): 1062-1064.
[6] Koivisto T, Vanninen R, Hurskainen H, et al. Outcomes of early endovascular versus surgical treatment of ruptured cerebral aneurysms: a prospective randomized study[J]. Stroke, 2000, 31(10): 2369-2377.
[7] Parolari A, Tremoli E, Cavallotti L, et al. Do statins improve outcomes and delay the progression of non-rheumatic calcific aortic stenosis[J]. Heart, 2011, 97(7): 523-529.
[8] van der Loo B, Spring S, Koppensteiner R. High-dose atorvastatin treatment in patients with peripheral arterial disease: effects on platelet aggregation, blood rheology and plasma homocysteine[J]. Clin Hemorheol Microcirc, 2011, 47(4): 241-251.
[9] 李建勇, 胡大一, 史旭波, 等. 不同剂量阿托伐他汀对冠心病患者的疗效和安全多中心研究[J]. 中华心血管病杂志, 2005, 33(12): 1085-1087.
[10] Takemoto M, Liao JK. Pleiotropic effects of 3-hydroxy-3-methyl-glutaryl cozezyme a reductase inhibitors[J]. Arterioscler Thromb Vasc Biol, 2001, 21(10): 1712-1719.
[11] 李悦妍, 关玉庆, 苗伟, 等. 阿托伐他汀对动脉粥样硬化模型兔toll样受体4及其下游信号表达的影响[J]. 山东大学学报:医学版, 2014, 52(6): 1-6. LI Yueyan, GUAN Yuqing, MIAO Wei, et al. Effect of atorvastatin on TLR4 expression and downstream signaling in atherosclerotic rabbits[J]. Journal of Shandong University: Health Sciences, 2014, 52(6): 1-6.
[12] Nissen SE, Nicholls SJ, Sipahi I, et al. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial[J]. JAMA, 2006, 295(13): 1556-1565.
[13] Leanne Satchell, David S. Oxidation of Low-density lipoprotein by Iron at lysosomal PH: implication for atherosclerosis[J]. Biochemistry, 2012, 51(18): 3767-3775.
[14] Ross R. Atherosclerosis-an inflammatory disease[J]. N Engl J Med, 1999, 340(2): 115-126.
[15] Thiele JR, Habersberger J, Braig D, et al. Dissociation of pentameric to monomeric C-reactive protein localizes and aggravates inflammation: in vivo proof of a powerful proinflammatory mechanism and a new anti-inflammatory strategy[J]. Circulation, 2014, 130(1): 35-50.
[16] Sigueira DA, Sousa AG, Costa Junior Jde R, et al. Correlation between plaque composition as assessed by virtual histology and C-reactive protein[J]. Arg Bras Cardiol, 2013, 101(1): 78-86.
[17] Koenig W. High-sensitivity C-reactive protein and atherosclerotic disease: from improved risk prediction to risk-guided therapy[J]. Int J Cardiol, 2013, 168(6): 5126-5134.
[18] Wang C, Yan J, Yang P, et al. The relationship between CD40 gene polymorphism and unstable coronary atherosclerotic plaques[J]. Clin Cardiol, 2010, 33(6): E55-60.
[19] Davies MJ. Pathophysiology of acute coronary syndrome[J]. Heart, 2000, 83: 361-366.
[20] Nissen SE, Yock P. Intravascular ultrasound: novel pathophysiological insights and current clinical applications[J]. Circulation, 2001, 103(4): 604-616.
[21] Escolar E, Weigold G, Fuisz A, et al. New imaging techniques for diagnosing coronary artery disease[J]. CAMJ, 2006, 174(8): 487-495.
[1] 付洁琦,张曼,张晓璐,李卉,陈红. Toll样受体4抑制过氧化物酶体增殖物激活受体γ加重血脂蓄积的分子机制[J]. 山东大学学报 (医学版), 2020, 1(7): 24-31.
[2] 尹妮,杨关林,姜钧文,王春田,王凤耀,贾连群,高晓宇,潘嘉祥,李芹,李佳,冯元洁,高玉竹,周鹤,张哲. 巴马小型猪冠状动脉粥样硬化模型的评价方法[J]. 山东大学学报（医学版）, 2017, 55(7): 1-5.
[3] 宋昱,毛洋,刘庆梅,乔磊,帖媛媛,鲁璐,张蕾. 通心络对兔腹主动脉粥样硬化易损斑块中三维应变的影响[J]. 山东大学学报（医学版）, 2017, 55(5): 1-7.
[4] 樊彦伟,严冬雪,招友. 富氢水对兔腰椎间盘退变的影响[J]. 山东大学学报（医学版）, 2017, 55(3): 38-42.
[5] 张云华,李杰. 颈动脉斑块内新生血管显影程度及血浆Lp-PLA2水平对急性脑梗死的临床诊断价值[J]. 山东大学学报（医学版）, 2017, 55(3): 112-116.
[6] 魏丹丹,张澄. 血管紧张素Ⅳ型受体过表达对早期动脉粥样硬化斑块形成的影响[J]. 山东大学学报（医学版）, 2016, 54(8): 1-5.
[7] 王丹,亓恒涛,孙书珍. 原发性肾病综合征儿童颈动脉结构和功能改变[J]. 山东大学学报（医学版）, 2016, 54(5): 88-91.
[8] 孙鹏飞,孟晓,张凯,黎莉. 抵抗素样分子 β在动脉粥样硬化斑块稳定性中的作用[J]. 山东大学学报（医学版）, 2016, 54(3): 1-4.
[9] 李雪丽,徐丽君. 以孤立性眩晕为首发症状的双侧对称性桥臂梗死1例[J]. 山东大学学报（医学版）, 2016, 54(12): 90-92.
[10] 王小飞, 王成伟, 王志刚, 丁璇, 王敏卿. 应用Enterprise支架治疗动脉粥样硬化性椎-基底动脉狭窄的探讨[J]. 山东大学学报（医学版）, 2015, 53(8): 44-48.
[11] 于昕, 刘晓静, 刘向群. 黄芩苷抑制ox-LDL诱导内皮细胞凋亡的作用[J]. 山东大学学报（医学版）, 2015, 53(5): 5-9.
[12] 段瑞生. 他汀对动脉粥样硬化的免疫调节及其在临床应用中的思考[J]. 山东大学学报（医学版）, 2015, 53(5): 1-4.
[13] 于磊, 李振. 白细胞介素33在脑血管病患者血清中的表达及其作用机制[J]. 山东大学学报（医学版）, 2015, 53(4): 75-79.
[14] 徐忠阳, 王立启, 徐振兴, 赵乾, 朱世明. RhoA/ROCK信号通路与原发性高血压患者血压变异性及颈动脉内膜中层厚度的相关性[J]. 山东大学学报（医学版）, 2015, 53(2): 48-51.
[15] 刘国明, 史浩, 程海超. DCE-MRI在颈动脉粥样硬化斑块新生血管定量测量中的应用[J]. 山东大学学报（医学版）, 2015, 53(12): 76-80.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
No Suggested Reading articles found!
版权所有 © 2018 《山东大学学报(医学版)》编辑部　
地址:山东大学科技期刊社（济南市历城区山大南路27号山东大学中心校区明德楼B座721室） 电话: 0531-88366918 E-mail: xbyxb@sdu.edu.cn
本系统由北京玛格泰克科技发展有限公司设计开发