高盐高脂摄入致动脉粥样硬化与重构及辛伐他汀阻断作用的实验研究
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摘要
目的探讨大鼠经高钠盐与高脂肪复合喂养后血压、血脂、主动脉构型变化和中层粥样硬化改变以及辛伐他汀的阻断作用
方法随机选取60只成年雄性SD大鼠,随机分为5组,分别为正常对照组(N组)、高脂摄入组(F组)、高盐摄入组(S组)、高盐高脂复合摄入组(SF组)、高盐高脂加辛伐他汀组(T)组,分别予以标准饲料(0.4%食盐与0.2%胆固醇)、高脂饲料(1.2%胆固醇,0.4%食盐)、高盐饲料(4.4%食盐、0.2%胆固醇)、高盐高脂复合饲料(4.4%食盐、1.2%胆固醇)及高盐高脂复合饲料加辛伐他汀(0.2mg／kg)喂养10周后,测量各组大鼠体重、鼠尾血压计测量动脉压、心率,处死动物后测定血清甘油三酯与总胆固醇的浓度；取主动脉环起始段,以10μm间隔厚度行冰冻切片进行油红0和苏木精染色观察动脉中层粥样硬化情况；常规苏木精-伊红染色计算动脉中膜层厚度与动脉内腔面积与血管腔总的面积比值。结果(1)FS组、F组、S组的收缩压分别为170.5±14.787 mmHg、148.95±27.383mmHg、156.4±18.010mmHg,舒张压为131.315±9.00mmHg、116.7±5.147mmHg、131.589±11.548 mmHg,与N组相比,上述三组血压明显增高(P<0.001),而T组与N组比较也增高(P<0.001),但较FS组明显降低,(P<0.05)。FS组心率(438.70±20.166次／分)与其他组比较明显增高(P<0.001),而F组与S组(411.4±19.132次／分、409.00±10.424次／分)与N组和T组比较,无显著差异；同样,N组比,FS组与F组体重明显高于N组(412.34±45.61g,390.86±35.55g,P<0.001),而T组体重则明显低于N组(344.48±27.59g,P<0.001),S组、FS组与F组之间未见明显差异。
(2)F组与FS组血脂总胆固醇明显增高(1.875±0.133 mmol／L、2.036±0.177 mmol／L),同时该两组甘油三酯也明显增高(1.062±0.070 mmol／L、1.256±0.085 mmol／L),与N组和T组比较明显升高(P<0.001),而S组与N组无明显差异。
(3)S组、F组与FS组大鼠动脉构型也明显异常,动脉中膜厚度为(135.28±12.29μm、158.86±15.23μm、184.00±13.40μm),与正常组比较明显增厚(P<0.001)；同时大鼠动脉内腔面积与血管腔总的面积比值也存在明显异常,FS组、F组动脉内腔面积／血管腔总面积比值明显减少(分别为66.7±6.91,72.9±4.90)与正常组比较明显变小(P＜0.05)。
(4)病理切片H-E染色中FS组均表现为中膜增厚,其中50%大鼠出现典型的动脉粥样硬化改变,油红0染色提示血管壁出现明显脂肪浸润；而同时F组大鼠亦表现为中膜增厚,但程度较FS组轻,仅30%出现粥样硬化斑块,油红0染色提示脂肪浸润；而S组与辛伐他汀治疗组无动脉粥样硬化改变,仅表现为中膜增厚。
结论1.通过高盐高脂复合刺激后,大鼠的血压明显升高,而复合刺激改变明显强于单一因素,表明通过高盐高脂喂养可以建立类似代谢异常所致的而高血压大鼠模型；
2.高盐高脂复合喂养的大鼠动脉发生动脉内膜呈内向型增厚和粥样硬化,可以制备代谢因素异常所致动脉粥样硬化模型,同样复合刺激改变明显强于单一因素；
3.他汀类药物对大鼠动脉血管重构和粥样硬化过程具备明显阻断作用。
Objective To study the changes of blood pressure,blood lipids,conformational changes and aortic atherosclerosis in rats after combined high salt and rich fat diet ingestion as well as the possible blocking role of simvastatin in process.
Method a total of 60 adult male SD rats were randomly divided into 5 grous, namely normal control group (N group),rich fat intake group (F group) and high salt intake group (S group), high salt with rich fat intake group (SF group),rich fat with high salt plus simvastatin group (T group) and were given standard diet (0.4%,0.2% salt and cholesterol), high fat diet (1.2% cholesterol,0.4% salt) high salt diet (4.4% salt,0.2% cholesterol), high salt compound fat diet (4.4% salt,1.2% cholesterol) and high salt with rich fat diet plus t simvastatin (0.2mg/kg) after 10 weeks measured weight,measured blood pressure, heart rate using tail-cuff sphygmomanometer of rats in each group, was collected to determine serum concentrations of triglyceride and total cholesterol; get ascending aortic root initial segment of aortic rings to 10μm thickness intervals do Frozen sections were oil red O and hematoxylin staining of the middle artery atherosclerosis situation; routine hematoxylin-eosin staining in the calculation of film thickness and arterial arterial lumen area and lumen area ratio of the total.
Results (1) FS group, F group, S group were systolic blood pressure (170.5±14.787 mmHg、148.95±27.383mmHg、160.4±18.010mmHg), diastolic blood pressure (131.315±9.00mmHg、116.7±5.147mmHg、131.589±11.548mmHg) compared with N group, the three blood pressure was significantly higher (P <0.001), while the T group compared with N group also increased, but significantly lower than the FS group, (P<0.05). FS group heart rate (38.70±20.166 beats/min) compared with the other group differences (P<0.001), while the F group and S group (411.4±19.132 beats/min,409.00±10.424beats/min) and the N group and the T group, no difference; Similarly, N group than, FS group and F group body weight was significantly higher than N group (412.34±45.61g,390.86±35.55g, P<0.001), whereas body weight was lower than T N group (344.48±27.59g, P<0.001), S group, FS group and no significant difference between the F group.
(2) F group and the FS fat group was significantly higher total cholesterol and blood lipid (1.875±0.133mmol/L,2.036±0.177mmol/L), while triglyceride was also significantly increased in the two groups (1.062, with the N group and T group was significantly higher (P<0.001), while the S group and N group no significant difference.
(3) S group, F group and the FS group was significantly abnormal arterial configuration, arterial medial thickness(135.28±12.29μm,158.86±15.23μm, 184.00±13.40μm),thickened with the normal group (P<0.001); while arterial lumen area and lumen area ratio of the total there are obvious exceptions, FS group, F Group artery lumen area/total area ratio was significantly decreased (66.7±6.91,72.9±4.90) compared with the N group was significantly smaller (P<0.05).
(4) HE staining of biopsy 50% FS group in rats the typical atherosclerotic changes in the membrane showed thickening of the remaining oil red O staining showed significant fatty infiltration of the vessel wall; while at the same group of 30% F atherosclerotic plaques occurs, oil red O staining showed fatty infiltration; the S group and simvastatin group without atherosclerotic changes, manifested in the film thickness.
Conclusion 1. The rat's blood pressure rise significantly after high salt or fat ingestion, which is enhanced by combined two factors, indicating the hypertensive rat model can be established by high salt with rich fat diet
2. Diet combined high salt and rich fat can induce arterial intima thickening and atherosclerosis,the pathologic process can be blocked by Statins, which simulate the clinic situation.
方法随机选取60只成年雄性SD大鼠,随机分为5组,分别为正常对照组(N组)、高脂摄入组(F组)、高盐摄入组(S组)、高盐高脂复合摄入组(SF组)、高盐高脂加辛伐他汀组(T)组,分别予以标准饲料(0.4%食盐与0.2%胆固醇)、高脂饲料(1.2%胆固醇,0.4%食盐)、高盐饲料(4.4%食盐、0.2%胆固醇)、高盐高脂复合饲料(4.4%食盐、1.2%胆固醇)及高盐高脂复合饲料加辛伐他汀(0.2mg／kg)喂养10周后,测量各组大鼠体重、鼠尾血压计测量动脉压、心率,处死动物后测定血清甘油三酯与总胆固醇的浓度；取主动脉环起始段,以10μm间隔厚度行冰冻切片进行油红0和苏木精染色观察动脉中层粥样硬化情况；常规苏木精-伊红染色计算动脉中膜层厚度与动脉内腔面积与血管腔总的面积比值。结果(1)FS组、F组、S组的收缩压分别为170.5±14.787 mmHg、148.95±27.383mmHg、156.4±18.010mmHg,舒张压为131.315±9.00mmHg、116.7±5.147mmHg、131.589±11.548 mmHg,与N组相比,上述三组血压明显增高(P<0.001),而T组与N组比较也增高(P<0.001),但较FS组明显降低,(P<0.05)。FS组心率(438.70±20.166次／分)与其他组比较明显增高(P<0.001),而F组与S组(411.4±19.132次／分、409.00±10.424次／分)与N组和T组比较,无显著差异；同样,N组比,FS组与F组体重明显高于N组(412.34±45.61g,390.86±35.55g,P<0.001),而T组体重则明显低于N组(344.48±27.59g,P<0.001),S组、FS组与F组之间未见明显差异。
(2)F组与FS组血脂总胆固醇明显增高(1.875±0.133 mmol／L、2.036±0.177 mmol／L),同时该两组甘油三酯也明显增高(1.062±0.070 mmol／L、1.256±0.085 mmol／L),与N组和T组比较明显升高(P<0.001),而S组与N组无明显差异。
(3)S组、F组与FS组大鼠动脉构型也明显异常,动脉中膜厚度为(135.28±12.29μm、158.86±15.23μm、184.00±13.40μm),与正常组比较明显增厚(P<0.001)；同时大鼠动脉内腔面积与血管腔总的面积比值也存在明显异常,FS组、F组动脉内腔面积／血管腔总面积比值明显减少(分别为66.7±6.91,72.9±4.90)与正常组比较明显变小(P＜0.05)。
(4)病理切片H-E染色中FS组均表现为中膜增厚,其中50%大鼠出现典型的动脉粥样硬化改变,油红0染色提示血管壁出现明显脂肪浸润；而同时F组大鼠亦表现为中膜增厚,但程度较FS组轻,仅30%出现粥样硬化斑块,油红0染色提示脂肪浸润；而S组与辛伐他汀治疗组无动脉粥样硬化改变,仅表现为中膜增厚。
结论1.通过高盐高脂复合刺激后,大鼠的血压明显升高,而复合刺激改变明显强于单一因素,表明通过高盐高脂喂养可以建立类似代谢异常所致的而高血压大鼠模型；
2.高盐高脂复合喂养的大鼠动脉发生动脉内膜呈内向型增厚和粥样硬化,可以制备代谢因素异常所致动脉粥样硬化模型,同样复合刺激改变明显强于单一因素；
3.他汀类药物对大鼠动脉血管重构和粥样硬化过程具备明显阻断作用。
Objective To study the changes of blood pressure,blood lipids,conformational changes and aortic atherosclerosis in rats after combined high salt and rich fat diet ingestion as well as the possible blocking role of simvastatin in process.
Method a total of 60 adult male SD rats were randomly divided into 5 grous, namely normal control group (N group),rich fat intake group (F group) and high salt intake group (S group), high salt with rich fat intake group (SF group),rich fat with high salt plus simvastatin group (T group) and were given standard diet (0.4%,0.2% salt and cholesterol), high fat diet (1.2% cholesterol,0.4% salt) high salt diet (4.4% salt,0.2% cholesterol), high salt compound fat diet (4.4% salt,1.2% cholesterol) and high salt with rich fat diet plus t simvastatin (0.2mg/kg) after 10 weeks measured weight,measured blood pressure, heart rate using tail-cuff sphygmomanometer of rats in each group, was collected to determine serum concentrations of triglyceride and total cholesterol; get ascending aortic root initial segment of aortic rings to 10μm thickness intervals do Frozen sections were oil red O and hematoxylin staining of the middle artery atherosclerosis situation; routine hematoxylin-eosin staining in the calculation of film thickness and arterial arterial lumen area and lumen area ratio of the total.
Results (1) FS group, F group, S group were systolic blood pressure (170.5±14.787 mmHg、148.95±27.383mmHg、160.4±18.010mmHg), diastolic blood pressure (131.315±9.00mmHg、116.7±5.147mmHg、131.589±11.548mmHg) compared with N group, the three blood pressure was significantly higher (P <0.001), while the T group compared with N group also increased, but significantly lower than the FS group, (P<0.05). FS group heart rate (38.70±20.166 beats/min) compared with the other group differences (P<0.001), while the F group and S group (411.4±19.132 beats/min,409.00±10.424beats/min) and the N group and the T group, no difference; Similarly, N group than, FS group and F group body weight was significantly higher than N group (412.34±45.61g,390.86±35.55g, P<0.001), whereas body weight was lower than T N group (344.48±27.59g, P<0.001), S group, FS group and no significant difference between the F group.
(2) F group and the FS fat group was significantly higher total cholesterol and blood lipid (1.875±0.133mmol/L,2.036±0.177mmol/L), while triglyceride was also significantly increased in the two groups (1.062, with the N group and T group was significantly higher (P<0.001), while the S group and N group no significant difference.
(3) S group, F group and the FS group was significantly abnormal arterial configuration, arterial medial thickness(135.28±12.29μm,158.86±15.23μm, 184.00±13.40μm),thickened with the normal group (P<0.001); while arterial lumen area and lumen area ratio of the total there are obvious exceptions, FS group, F Group artery lumen area/total area ratio was significantly decreased (66.7±6.91,72.9±4.90) compared with the N group was significantly smaller (P<0.05).
(4) HE staining of biopsy 50% FS group in rats the typical atherosclerotic changes in the membrane showed thickening of the remaining oil red O staining showed significant fatty infiltration of the vessel wall; while at the same group of 30% F atherosclerotic plaques occurs, oil red O staining showed fatty infiltration; the S group and simvastatin group without atherosclerotic changes, manifested in the film thickness.
Conclusion 1. The rat's blood pressure rise significantly after high salt or fat ingestion, which is enhanced by combined two factors, indicating the hypertensive rat model can be established by high salt with rich fat diet
2. Diet combined high salt and rich fat can induce arterial intima thickening and atherosclerosis,the pathologic process can be blocked by Statins, which simulate the clinic situation.
引文
1. Peter Libby, Paul M. Ridker and Attilio Maseri Inflammation and Atherosclerosis[J] Circulation 2002;105;1135-1143.
2. Henry C. McGill, Jr, C. Alex McMahan etal. Preventing Heart Disease in the 21st Century:Implications of the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study[J] Circulation 2008;117;1216-1227.
3. Pedro R. Moreno, MD; K-Raman Purushothaman, MD; Marc Sirol, MD,etal. Neovascularization in Human Atherosclerosis [J] Circulation. 2006;113:2245-2252.
4. Ulf Landmesser, MD; Burkhard Hornig, MD; Helmut Drexler, MD Endothelial Function:A Critical Determinant in Atherosclerosis?[J] Circulation 2004;109;Ⅱ-27-Ⅱ-33.
5.蔡志友晏勇氧化型低密度脂蛋白致动脉粥样硬化的机制[J]中国卒中杂志2008年3月第3卷第3期187-190.
6.Tanika N.Kelly,Dongfeng Gu,Jing Chen,etal.Hypertension Subtype and Risk of Cardiovascular Disease in Chinese Adults[J] Circulation 2008;118;1558-1566.
7.YangfengYu,RachelHuxley,LimingLi,etal.Prevalence,Awarenass,Treatment,a nd Control of Hypertension in China:data from the China National Nutrion Health Survey 2002[J] circulation 2008;118;2679-2686.
8.R. Wayne Alexander. Hypertension and the Pathogenesis of Atherosclerosis:Oxidative Stress and the Mediation of Arterial Inflammatory Response:A New Perspective [J] Hypertension.1995;25:155-161.
9.内科学／陆再英等主编.——7版。——北京：人民卫生出版社,2008.1,811页。
10.Simgh U,Devaraj S,Jialal I etal.Comparsion Effect of Atorvastion(10 versus
80 mg) on biomarkers of Inflammation and Oxidative Stress in Subjects With Metabolic Syndrome[J] Am J Cardiol,2008,102(3);321-325.
11. WILLIAM J K, SUKHOVA G K, HERRINGTON D M, et al. Pravastatin Has Cholesterol-Lowering Independent Effects on the Artery Wall of Atherosclerotic Monkeys[J] J Am Coll Car-diol,1998,31:684-691.
12.Juan Rodriguez-Vita, Eva Sanchez-Galan, Beatriz Santamaria etal.Essential Role of TGF-P/Smad Pathway on Statin Dependent VascularSmoothMuscleCellRegulation[J].H.oSOne,2008,(13):E3959.
13.Eduardo Pimenta; Krishna K. Gaddam; Suzanne Oparil etal. Effects of Dietary Sodium Reduction on Blood Pressure in Subjects With Resistant Hypertension[J]. Hypertension 2009;54:475.
14. Alain Tedgui; Ziad Mallat.Hypertension:A Novel Regulator of Adaptive Immunity in atherosclerosis?[J]. Hypertension 2004;44:257
15. Wolfgang Koenig, MD; Natalie Khuseyinova, MD; Hannelore Lowel, MD et al. Lipoprotein-Associated Phospholipase A2 Adds to Risk Prediction of Incident Coronary Events by C-Reactive Protein in Apparently Healthy Middle-Aged Men From the General Population:Results From the 14-Year Follow-Up of a Large Cohort From Southern Germany[J] Circulation 2004;110;1903-1908.
16. Masao Kakoki, Yasunobu Hirata, Hiroshi Hayakawa et al. Effects of Hypertension, Diabetes Mellitus, and Hypercholesterolemia on Endothelin Type B Receptor-Mediated Nitric Oxide Release From Rat Kidney [J] Circulation 1999;99;1242-1248.
17.傅仁彪,陈林,李朝品,等.肾素-血管紧张素-醛固酮系统与矿工高血压的初步研究[J].中国病理生理杂志,2001,17(12)：1175-1178.
18. Daniele Versari, Mario Gossl, Dallit Mannheim, etal. Hypertension and Hypercholesterolemia Differentially Affect the Function and Structure of Pig Carotid Artery[J] Hypertension Dec 2007; 50:1063-1068.
19.Semin Fenkci, Veysel Fenkci, Mehmet Yilmazer etal. Effects of short-term transdermal hormone replacement therapy on glycaemic control, lipid metabolism, C-reactive protein and proteinuria in postmenopausal women with type 2 diabetes or hypertension[J] Human Reproduction Vol.18, No.4 pp. 866-870,2003
20. B. M. Schamberger, H. C. Geiss, M. M. Ritter et al. Influence of LDL apheresis on LDL subtypes in patients with coronary heart disease and severe hyperlipoproteinemia[J] Journal of Lipid Research Volume 41,2000.
21. Maqsood M. Elahi, Felino R. Cagampang, Frederick W. Anthony etal. Statin Treatment in Hypercholesterolemic Pregnant Mice Reduces Cardiovascular Risk Factors in Their Offspring[J] Hypertension 2008;51;939-944.
22. James K. Liao. Statin Therapy:Having the Good Without the Bad[J] Hypertension 2004;43;1171-1172.
23. 姚品芳,钱禹林,范红心等.降脂治疗对心率变异性影响的临床研究[J].实用生理学杂志2009年18卷4期278-279.
24.Julia Steinberger, Stephen R. Daniels, Robert H. Eckel etal. Progress and Challenges in Metabolic Syndrome in Children and Adolescents:A Scientific Statement From the American Heart Association Atherosclerosis Hypertension, and obesity in the Young Committee of the Council on Cardiovascular Disease in the Young; Council on Cardiovascular Nursing; and Council on Nutrition, Physical Activity, and Metabolism[J]. Circulation, Feb 2009; 119:628-647.
25. Kwang Kon Koh, Michael J. Quon, Seung Hwan Han etal. Additive Beneficial Effects of Losartan Combined With Simvastatin in the Treatment of Hypercholesterolemic, Hypertensive Patients[J]. Circulation, Dec 2004; 110: 3687-3692.
26. Robert A. Koza, Larissa Nikonova, Jessica Hogan, etal. Changes in gene expression foreshadow diet—induced obesity in genetically identical mice[J]. PLoS Genetics,2006,2(5):81.
27. Herve Duplain, Remy Burcelin, Claudio Sartori etal. Insulin Resistance, hyperlipidemia, and Hypertension in Mice Lacking Endothelial Nitric Oxide SynthaseNote Added in Proof[J]. Circulation, Sep 1998; 98:1291-1296.
28. Murray Esler, Nora Straznicky, Nina Eikelis etal. Mechanisms of Sympathetic Activation in Obesity-Related Hypertension[J]. Hypertension, Nov 2006; 48:787-796.
29.包艳红,许秀举,王强.高脂血症与膳食营养及其相关因素的研究新进展[J].包头医学院学报第25卷79-80.
30. Nicholas J. Leeper, Reza Ardehali etal. Statin Use in Patients With Extremely Low Low-Density Lipoprotein Levels Is Associated With Improved Survival[J]. Circulation, Aug 2007; 116:613-618.
31. Sullivan, Ralph A.H. Stewart, Wendy Hague etal. Relationship Between Lipid Levels and Clin ical Outcomes in the Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) Trial:To What Extent Is the Reduction in Coronary Events with pravasstatin Explained by On-Study Lipid Levels?[J]. Circulation, Mar 2002; 105:1162-1169.
32. Rouleau, David T. Nash, Marc A. Pfeffer etal. Relationship Between Plasma LDL Concentrations During Treatment With Pravastatin and Rcurrent Coronary Events in the Cholesterol and Recurrent Events Trial[J]. Circulation, Apr 1998; 97:1446-1452.
33. C. Rae. A. Graham Human resistin promotes macrophage lipid accumulation[J] Diabetologia (2006) 49:1112-1114.
34. Sven Wassmann, Thomas Czech, Martin van Eickels etal. Inhibition of Diet-Induced Atherosclerosis and Endothelial Dysfunction in Apolipoprotein E/Angiotensin II Type 1A Receptor Double-Knockout Mice [J]. Circulation, Nov 2004; 110:3062-3067.
35. Katherine E. Lewis, Elizabeth A. Kirk, Thomas O. McDonald etal. Increase in Serum Amyloid A Evoked by Dietary Cholesterol Is Associated With Increased atherosclerosis in Mice[J]. Circulation, Aug 2004; 110:540-545.
36. Ulf Landmesser, MD; Burkhard Hornig, MD; Helmut Drexler, MD Endothelial Function:A Critical Determinant in Atherosclerosis?[J] Circulation 2004;109;Ⅱ-27-Ⅱ-33.
37. Lu, Hong; Cassis, Lisa A.; Daugherty, Alan Atherosclerosis and Arterial Blood Pressure in Mice.[J]. Current Drug Targets Volume 8, Number 11, November 2007, pp.1181-1189(9).
38. Uichi Ikeda, Masahisa Shimpo, Yoshiaki Murakami etal. Peroxisome Proliferator-Activated Receptor-(?) Ligands Inhibit Nitric Oxide Synthesis in Vascular Smooth Muscle Cells[J]. Hypertension, Jun 2000; 35:1232-1236.
39. Rodolfo Paoletti, Antonio M. Gotto, Jr etal. Inflammation in Atherosclerosis and Implications for Therapy[J]. Circulation, Jun 2004; 109:Ⅲ-20-Ⅲ-26.
40.宋兴辉,周海鸥,孙阳等.高脂高胆固醇饮食对3基因突变小鼠动脉粥样硬化病变的影响[J].中国病理生理学杂志2009,25(10)：1887-1991.
41. Steffi Kopprasch, Jens Pietzsch, Eberhard Kuhlisch etal. In Vivo Evidence for Increased Oxidation of Circulating LDL in Impaired Glucose Tolerance [J]. Diabetes October 2002 vol.51 no.10 3102-3106.
42. Julian P.J. Halcox and John E. Deanfield. Beyond the Laboratory:Clinical Implications for statin Pleiotropy[J] Circulation, Jun 2004; 109:Ⅱ-42-Ⅱ-48. 43. Allen J. Taylor, Lance E. Sullenberger, Hyun J. Lee etal. Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER) 2:A Double-Blind, Placebo-Controlled Study of Extended-Release Niacin on Atherosclerosis Progression in Secondary Prevention Patients Treated With statins[J]. Circulation, Dec 2004; 110:3512-3517.
1. Peter Libby, Paul M. Ridker and Attilio Maseri Inflammation and Atherosclerosis[J] Circulation 2002;105;1135-1143.
2.李薇,杜军保 脉粥样硬化发病机制研究进展{J} 儿科临床杂志12009.2411}：58—6.
3. Christian C.Haudenschild Pathogenesis of Atherosclerosis::State of the A rt[J] Cardiovascular Drugs and Therapy 4:998-1004,1999.
4. Jean Davignon and Peter Ganz Role of Endothelial Dysfunction in Atherosclerosis [J] Circulation 2004;109;Ⅲ-27-Ⅲ-32.
5. Ulf Landmesser, MD; Burkhard Hornig, MD; Helmut Drexler, MD Endothelial Function:A Critical Determinant in Atherosclerosis?[J] Circulation 2004;109;Ⅱ-27-Ⅱ-33.
[6]蔡志友 晏勇 氧化型低密度脂蛋白致动脉粥样硬化的机制[J] 中国卒中杂志 2008年3月 第3卷 第3期 187-190.
[7]John E. Deanfield, Julian P. Halcox and Ton J. Rabelink Endothelial Function and Dysfunction:Testing and Clinical Relevance[J] Circulation 2007;115;1285-1295.
[8]Robert M. F. Wever, Thomas F. Luscher, Francesco Cosentino and Ton J. Rabelink Atherosclerosis and the Two Faces of Endothelial Nitric Oxide Synthase[J] Circulation 1998;97;108-112.
[9]Renate Schnabel and Stefan Blankenberg Oxidative Stress in Cardiovascular Disease Successful Translation From Bench to Bedside? [J] Circulation 2007;116;1338-1340.
[10]舒筱灿 吴和平 韩伟 舒旭NADPH氧化酶对动脉粥样硬化兔氧化应激的影响[J]实用预防医学2007年6月 第14卷第3期.
[11]陈瑗 周玫 氧化应激-炎症在动脉粥样硬化发生发展中作用研究的 新进展[J]中国动脉硬化杂志2008年第16卷第10期
[12]Kathy K. Griendling and Garret A. FitzGerald Oxidative Stress and Cardiovascular Injury:Part I:Basic Mechanisms and In Vivo Monitoring of ROS[J] Circulation 2003;108;1912-1916.
[13]Peter Libby, Paul M. Ridker and Attilio Maseri Inflammation and Atherosclerosis[J] Circulation 2002;105;1135-1143.
[14]Goran K. Hansson, Peter Libby, Uwe Schonbeck and Zhong-Qun Yan Innate and Adaptive Immunity in the Pathogenesis of Atherosclerosis[J] Circ. Res.2002;91;281-291.
[15]C. Rae. A. Graham Human resistin promotes macrophage lipid accumulation[J] Diabetologia (2006) 49:1112-1114.
[16]Hye Seung Jung, Ki-Ho Park, Young Min Cho, Sung Soo Chung,Hyun Ju Cho, Soo Youn Cho, Sang Joon Kim, Seong Yeon Kim,Hong Kyu Lee, Kyong Soo Park Resistin is secreted from macrophages in atheromas and promotes atherosclerosis[J] Cardiovascular Research 69 (2006) 76-85.
[17]F. Angelico. C. Alessandri. D. Ferro et al. Enhanced soluble CD40L in patients with the metabolic syndrome:relationship with in vivo thrombin generation[J] Diabetologia (2006) 49:1169-1174.
18. Jae-Kwan Cha et al. Changes in Platelet P-Selectin and in Plasma C-Reactive Protein in Acute Atherosclerotic Ischemic Stroke Treated with a Loading Dose of Clopidogrel[J] Journal of Thrombosis and Thrombolysis 14(2), 145-150,2002.
[19]hu Q. Liu, Dalin Tang et al. Pattern formation of vascular smooth muscle cells subject to nonuniform fluid shear stress:mediation by gradient of cell density[J] Am J Physiol Heart Circ Physiol 285:H1072-H1080,2003.
[20]Kristopher S Cunninghaml and Avrum I Gotlieb The role of shear stress in the pathogenesis of atherosclerosis[J] Laboratory Investigation (2005) 85, 9-23.
[21]C. Michael Gross, Stephan Gerbaulet et al. Angiotensin II type 1 receptor expression in human coronary arteries with variable degrees of atherosclerosis[J] Basic Res Cardiol 97:327-333 (2002).
[22]Sivaramaprasad Gudi Ivana Huvar Charles R. White et al. Rapid activation of Ras by G alpha(q)and G beta gamma sub—units of heterotrimeric G proteins in human endothelial cells[J]. Arterioscler Thromb Vasc Biol,2003,23(6): 994—1000.
[23]Yi Liu, Benjamin P.-C. Chen, Min Lu et al. Shear Stress Activation of SREBP1 in Endothelial Cells Is Mediated by Integrins[J] Arterioscler. Thromb. Vasc. Biol.2002;22;76-81.
[24]D. Dean Potter, Christopher G. Sobey et al. Evidence That Macrophages in Atherosclerotic Lesions Contain Angiotensin II[J] Circulation1998;98;800-807.
[25]董晓雁,张桂清,方向明,郑民安,胡继军,林桂珍,蒋雯 卡托普利对动脉粥样硬化家兔内皮素和血管紧张素II的影响及其与原癌基因c-myc和c-fos的相关关系[J]中国动脉硬化杂志2002年第10卷第3期。
[26]Arthur M. Feldman, Gary S. Francis et al. 2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults:A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation[J] Circulation 2009;119;1977-2016.
[27]Sidney C. Smith, Jr, Jerilyn Allen et al. AHA/ACC Guidelines for Secondary Prevention for Patients With Coronary and Other Atherosclerotic Vascular Disease:2006 Update:Endorsed by the National Heart, Lung, and Blood Institute[J] Circulation 2006;113;2363-2372.
[28]中国成人血脂异常防治指南制定联合委员会中国成人血脂异常防治指南[J]中华心血管病杂志2007年5月第35卷第5期。
[29]Rodolfo Paoletti, Antonio M. Gotto et al. Inflammation in Atherosclerosis and Implications for Therapy[J] Circulation 2004;109;Ⅲ-20-Ⅲ-26.
[30]Joao A.C. Lima, Milind Y. Desai et al. Statin-Induced Cholesterol Lowering and Plaque Regression After 6 Months of Magnetic Resonance
Imaging-Monitored Therapy[J] Circulation 2004; 110;2336-2341.
[31]毛焕元心脏病学／毛焕元主编.-2版.-北京：人民卫生出版社,20001017页。
[32]Yasushi Ishigaki, Hideki Katagiri et al. Impact of Plasma Oxidized Low-Density Lipoprotein Removal on Atherosclerosis[J] Circulation 2008;118;75-83.
[33]Tillmann Cyrus Yuemang Yao et al. Vitamin E Reduces Progression of Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient Mice With Established Vascular Lesions[J] Circulation 2003;107;521-523.
[34]Syed Husain, Neil P. Andrews et al. Aspirin Improves Endothelial Dysfunction in Atherosclerosis[J] Circulation 1998;97;716-720.
[35]中国高血压防治指南修订委员会中国高血压防治指南(2005年修订版全文)2005.
[36]Linda Brookes, MSc ESH'07:New Consensus Hypertension Guidelines From the European Society of Hypertension/European Society of Cardiology (ESH/ESC) 2007.
[37]胡高文,程晓昱 中医药防治动脉粥样硬化的研究进展[J]中西医结合心脑血管病杂志2009年2月第7巷第2期.
2. Henry C. McGill, Jr, C. Alex McMahan etal. Preventing Heart Disease in the 21st Century:Implications of the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study[J] Circulation 2008;117;1216-1227.
3. Pedro R. Moreno, MD; K-Raman Purushothaman, MD; Marc Sirol, MD,etal. Neovascularization in Human Atherosclerosis [J] Circulation. 2006;113:2245-2252.
4. Ulf Landmesser, MD; Burkhard Hornig, MD; Helmut Drexler, MD Endothelial Function:A Critical Determinant in Atherosclerosis?[J] Circulation 2004;109;Ⅱ-27-Ⅱ-33.
5.蔡志友晏勇氧化型低密度脂蛋白致动脉粥样硬化的机制[J]中国卒中杂志2008年3月第3卷第3期187-190.
6.Tanika N.Kelly,Dongfeng Gu,Jing Chen,etal.Hypertension Subtype and Risk of Cardiovascular Disease in Chinese Adults[J] Circulation 2008;118;1558-1566.
7.YangfengYu,RachelHuxley,LimingLi,etal.Prevalence,Awarenass,Treatment,a nd Control of Hypertension in China:data from the China National Nutrion Health Survey 2002[J] circulation 2008;118;2679-2686.
8.R. Wayne Alexander. Hypertension and the Pathogenesis of Atherosclerosis:Oxidative Stress and the Mediation of Arterial Inflammatory Response:A New Perspective [J] Hypertension.1995;25:155-161.
9.内科学／陆再英等主编.——7版。——北京：人民卫生出版社,2008.1,811页。
10.Simgh U,Devaraj S,Jialal I etal.Comparsion Effect of Atorvastion(10 versus
80 mg) on biomarkers of Inflammation and Oxidative Stress in Subjects With Metabolic Syndrome[J] Am J Cardiol,2008,102(3);321-325.
11. WILLIAM J K, SUKHOVA G K, HERRINGTON D M, et al. Pravastatin Has Cholesterol-Lowering Independent Effects on the Artery Wall of Atherosclerotic Monkeys[J] J Am Coll Car-diol,1998,31:684-691.
12.Juan Rodriguez-Vita, Eva Sanchez-Galan, Beatriz Santamaria etal.Essential Role of TGF-P/Smad Pathway on Statin Dependent VascularSmoothMuscleCellRegulation[J].H.oSOne,2008,(13):E3959.
13.Eduardo Pimenta; Krishna K. Gaddam; Suzanne Oparil etal. Effects of Dietary Sodium Reduction on Blood Pressure in Subjects With Resistant Hypertension[J]. Hypertension 2009;54:475.
14. Alain Tedgui; Ziad Mallat.Hypertension:A Novel Regulator of Adaptive Immunity in atherosclerosis?[J]. Hypertension 2004;44:257
15. Wolfgang Koenig, MD; Natalie Khuseyinova, MD; Hannelore Lowel, MD et al. Lipoprotein-Associated Phospholipase A2 Adds to Risk Prediction of Incident Coronary Events by C-Reactive Protein in Apparently Healthy Middle-Aged Men From the General Population:Results From the 14-Year Follow-Up of a Large Cohort From Southern Germany[J] Circulation 2004;110;1903-1908.
16. Masao Kakoki, Yasunobu Hirata, Hiroshi Hayakawa et al. Effects of Hypertension, Diabetes Mellitus, and Hypercholesterolemia on Endothelin Type B Receptor-Mediated Nitric Oxide Release From Rat Kidney [J] Circulation 1999;99;1242-1248.
17.傅仁彪,陈林,李朝品,等.肾素-血管紧张素-醛固酮系统与矿工高血压的初步研究[J].中国病理生理杂志,2001,17(12)：1175-1178.
18. Daniele Versari, Mario Gossl, Dallit Mannheim, etal. Hypertension and Hypercholesterolemia Differentially Affect the Function and Structure of Pig Carotid Artery[J] Hypertension Dec 2007; 50:1063-1068.
19.Semin Fenkci, Veysel Fenkci, Mehmet Yilmazer etal. Effects of short-term transdermal hormone replacement therapy on glycaemic control, lipid metabolism, C-reactive protein and proteinuria in postmenopausal women with type 2 diabetes or hypertension[J] Human Reproduction Vol.18, No.4 pp. 866-870,2003
20. B. M. Schamberger, H. C. Geiss, M. M. Ritter et al. Influence of LDL apheresis on LDL subtypes in patients with coronary heart disease and severe hyperlipoproteinemia[J] Journal of Lipid Research Volume 41,2000.
21. Maqsood M. Elahi, Felino R. Cagampang, Frederick W. Anthony etal. Statin Treatment in Hypercholesterolemic Pregnant Mice Reduces Cardiovascular Risk Factors in Their Offspring[J] Hypertension 2008;51;939-944.
22. James K. Liao. Statin Therapy:Having the Good Without the Bad[J] Hypertension 2004;43;1171-1172.
23. 姚品芳,钱禹林,范红心等.降脂治疗对心率变异性影响的临床研究[J].实用生理学杂志2009年18卷4期278-279.
24.Julia Steinberger, Stephen R. Daniels, Robert H. Eckel etal. Progress and Challenges in Metabolic Syndrome in Children and Adolescents:A Scientific Statement From the American Heart Association Atherosclerosis Hypertension, and obesity in the Young Committee of the Council on Cardiovascular Disease in the Young; Council on Cardiovascular Nursing; and Council on Nutrition, Physical Activity, and Metabolism[J]. Circulation, Feb 2009; 119:628-647.
25. Kwang Kon Koh, Michael J. Quon, Seung Hwan Han etal. Additive Beneficial Effects of Losartan Combined With Simvastatin in the Treatment of Hypercholesterolemic, Hypertensive Patients[J]. Circulation, Dec 2004; 110: 3687-3692.
26. Robert A. Koza, Larissa Nikonova, Jessica Hogan, etal. Changes in gene expression foreshadow diet—induced obesity in genetically identical mice[J]. PLoS Genetics,2006,2(5):81.
27. Herve Duplain, Remy Burcelin, Claudio Sartori etal. Insulin Resistance, hyperlipidemia, and Hypertension in Mice Lacking Endothelial Nitric Oxide SynthaseNote Added in Proof[J]. Circulation, Sep 1998; 98:1291-1296.
28. Murray Esler, Nora Straznicky, Nina Eikelis etal. Mechanisms of Sympathetic Activation in Obesity-Related Hypertension[J]. Hypertension, Nov 2006; 48:787-796.
29.包艳红,许秀举,王强.高脂血症与膳食营养及其相关因素的研究新进展[J].包头医学院学报第25卷79-80.
30. Nicholas J. Leeper, Reza Ardehali etal. Statin Use in Patients With Extremely Low Low-Density Lipoprotein Levels Is Associated With Improved Survival[J]. Circulation, Aug 2007; 116:613-618.
31. Sullivan, Ralph A.H. Stewart, Wendy Hague etal. Relationship Between Lipid Levels and Clin ical Outcomes in the Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) Trial:To What Extent Is the Reduction in Coronary Events with pravasstatin Explained by On-Study Lipid Levels?[J]. Circulation, Mar 2002; 105:1162-1169.
32. Rouleau, David T. Nash, Marc A. Pfeffer etal. Relationship Between Plasma LDL Concentrations During Treatment With Pravastatin and Rcurrent Coronary Events in the Cholesterol and Recurrent Events Trial[J]. Circulation, Apr 1998; 97:1446-1452.
33. C. Rae. A. Graham Human resistin promotes macrophage lipid accumulation[J] Diabetologia (2006) 49:1112-1114.
34. Sven Wassmann, Thomas Czech, Martin van Eickels etal. Inhibition of Diet-Induced Atherosclerosis and Endothelial Dysfunction in Apolipoprotein E/Angiotensin II Type 1A Receptor Double-Knockout Mice [J]. Circulation, Nov 2004; 110:3062-3067.
35. Katherine E. Lewis, Elizabeth A. Kirk, Thomas O. McDonald etal. Increase in Serum Amyloid A Evoked by Dietary Cholesterol Is Associated With Increased atherosclerosis in Mice[J]. Circulation, Aug 2004; 110:540-545.
36. Ulf Landmesser, MD; Burkhard Hornig, MD; Helmut Drexler, MD Endothelial Function:A Critical Determinant in Atherosclerosis?[J] Circulation 2004;109;Ⅱ-27-Ⅱ-33.
37. Lu, Hong; Cassis, Lisa A.; Daugherty, Alan Atherosclerosis and Arterial Blood Pressure in Mice.[J]. Current Drug Targets Volume 8, Number 11, November 2007, pp.1181-1189(9).
38. Uichi Ikeda, Masahisa Shimpo, Yoshiaki Murakami etal. Peroxisome Proliferator-Activated Receptor-(?) Ligands Inhibit Nitric Oxide Synthesis in Vascular Smooth Muscle Cells[J]. Hypertension, Jun 2000; 35:1232-1236.
39. Rodolfo Paoletti, Antonio M. Gotto, Jr etal. Inflammation in Atherosclerosis and Implications for Therapy[J]. Circulation, Jun 2004; 109:Ⅲ-20-Ⅲ-26.
40.宋兴辉,周海鸥,孙阳等.高脂高胆固醇饮食对3基因突变小鼠动脉粥样硬化病变的影响[J].中国病理生理学杂志2009,25(10)：1887-1991.
41. Steffi Kopprasch, Jens Pietzsch, Eberhard Kuhlisch etal. In Vivo Evidence for Increased Oxidation of Circulating LDL in Impaired Glucose Tolerance [J]. Diabetes October 2002 vol.51 no.10 3102-3106.
42. Julian P.J. Halcox and John E. Deanfield. Beyond the Laboratory:Clinical Implications for statin Pleiotropy[J] Circulation, Jun 2004; 109:Ⅱ-42-Ⅱ-48. 43. Allen J. Taylor, Lance E. Sullenberger, Hyun J. Lee etal. Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER) 2:A Double-Blind, Placebo-Controlled Study of Extended-Release Niacin on Atherosclerosis Progression in Secondary Prevention Patients Treated With statins[J]. Circulation, Dec 2004; 110:3512-3517.
1. Peter Libby, Paul M. Ridker and Attilio Maseri Inflammation and Atherosclerosis[J] Circulation 2002;105;1135-1143.
2.李薇,杜军保 脉粥样硬化发病机制研究进展{J} 儿科临床杂志12009.2411}：58—6.
3. Christian C.Haudenschild Pathogenesis of Atherosclerosis::State of the A rt[J] Cardiovascular Drugs and Therapy 4:998-1004,1999.
4. Jean Davignon and Peter Ganz Role of Endothelial Dysfunction in Atherosclerosis [J] Circulation 2004;109;Ⅲ-27-Ⅲ-32.
5. Ulf Landmesser, MD; Burkhard Hornig, MD; Helmut Drexler, MD Endothelial Function:A Critical Determinant in Atherosclerosis?[J] Circulation 2004;109;Ⅱ-27-Ⅱ-33.
[6]蔡志友 晏勇 氧化型低密度脂蛋白致动脉粥样硬化的机制[J] 中国卒中杂志 2008年3月 第3卷 第3期 187-190.
[7]John E. Deanfield, Julian P. Halcox and Ton J. Rabelink Endothelial Function and Dysfunction:Testing and Clinical Relevance[J] Circulation 2007;115;1285-1295.
[8]Robert M. F. Wever, Thomas F. Luscher, Francesco Cosentino and Ton J. Rabelink Atherosclerosis and the Two Faces of Endothelial Nitric Oxide Synthase[J] Circulation 1998;97;108-112.
[9]Renate Schnabel and Stefan Blankenberg Oxidative Stress in Cardiovascular Disease Successful Translation From Bench to Bedside? [J] Circulation 2007;116;1338-1340.
[10]舒筱灿 吴和平 韩伟 舒旭NADPH氧化酶对动脉粥样硬化兔氧化应激的影响[J]实用预防医学2007年6月 第14卷第3期.
[11]陈瑗 周玫 氧化应激-炎症在动脉粥样硬化发生发展中作用研究的 新进展[J]中国动脉硬化杂志2008年第16卷第10期
[12]Kathy K. Griendling and Garret A. FitzGerald Oxidative Stress and Cardiovascular Injury:Part I:Basic Mechanisms and In Vivo Monitoring of ROS[J] Circulation 2003;108;1912-1916.
[13]Peter Libby, Paul M. Ridker and Attilio Maseri Inflammation and Atherosclerosis[J] Circulation 2002;105;1135-1143.
[14]Goran K. Hansson, Peter Libby, Uwe Schonbeck and Zhong-Qun Yan Innate and Adaptive Immunity in the Pathogenesis of Atherosclerosis[J] Circ. Res.2002;91;281-291.
[15]C. Rae. A. Graham Human resistin promotes macrophage lipid accumulation[J] Diabetologia (2006) 49:1112-1114.
[16]Hye Seung Jung, Ki-Ho Park, Young Min Cho, Sung Soo Chung,Hyun Ju Cho, Soo Youn Cho, Sang Joon Kim, Seong Yeon Kim,Hong Kyu Lee, Kyong Soo Park Resistin is secreted from macrophages in atheromas and promotes atherosclerosis[J] Cardiovascular Research 69 (2006) 76-85.
[17]F. Angelico. C. Alessandri. D. Ferro et al. Enhanced soluble CD40L in patients with the metabolic syndrome:relationship with in vivo thrombin generation[J] Diabetologia (2006) 49:1169-1174.
18. Jae-Kwan Cha et al. Changes in Platelet P-Selectin and in Plasma C-Reactive Protein in Acute Atherosclerotic Ischemic Stroke Treated with a Loading Dose of Clopidogrel[J] Journal of Thrombosis and Thrombolysis 14(2), 145-150,2002.
[19]hu Q. Liu, Dalin Tang et al. Pattern formation of vascular smooth muscle cells subject to nonuniform fluid shear stress:mediation by gradient of cell density[J] Am J Physiol Heart Circ Physiol 285:H1072-H1080,2003.
[20]Kristopher S Cunninghaml and Avrum I Gotlieb The role of shear stress in the pathogenesis of atherosclerosis[J] Laboratory Investigation (2005) 85, 9-23.
[21]C. Michael Gross, Stephan Gerbaulet et al. Angiotensin II type 1 receptor expression in human coronary arteries with variable degrees of atherosclerosis[J] Basic Res Cardiol 97:327-333 (2002).
[22]Sivaramaprasad Gudi Ivana Huvar Charles R. White et al. Rapid activation of Ras by G alpha(q)and G beta gamma sub—units of heterotrimeric G proteins in human endothelial cells[J]. Arterioscler Thromb Vasc Biol,2003,23(6): 994—1000.
[23]Yi Liu, Benjamin P.-C. Chen, Min Lu et al. Shear Stress Activation of SREBP1 in Endothelial Cells Is Mediated by Integrins[J] Arterioscler. Thromb. Vasc. Biol.2002;22;76-81.
[24]D. Dean Potter, Christopher G. Sobey et al. Evidence That Macrophages in Atherosclerotic Lesions Contain Angiotensin II[J] Circulation1998;98;800-807.
[25]董晓雁,张桂清,方向明,郑民安,胡继军,林桂珍,蒋雯 卡托普利对动脉粥样硬化家兔内皮素和血管紧张素II的影响及其与原癌基因c-myc和c-fos的相关关系[J]中国动脉硬化杂志2002年第10卷第3期。
[26]Arthur M. Feldman, Gary S. Francis et al. 2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults:A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation[J] Circulation 2009;119;1977-2016.
[27]Sidney C. Smith, Jr, Jerilyn Allen et al. AHA/ACC Guidelines for Secondary Prevention for Patients With Coronary and Other Atherosclerotic Vascular Disease:2006 Update:Endorsed by the National Heart, Lung, and Blood Institute[J] Circulation 2006;113;2363-2372.
[28]中国成人血脂异常防治指南制定联合委员会中国成人血脂异常防治指南[J]中华心血管病杂志2007年5月第35卷第5期。
[29]Rodolfo Paoletti, Antonio M. Gotto et al. Inflammation in Atherosclerosis and Implications for Therapy[J] Circulation 2004;109;Ⅲ-20-Ⅲ-26.
[30]Joao A.C. Lima, Milind Y. Desai et al. Statin-Induced Cholesterol Lowering and Plaque Regression After 6 Months of Magnetic Resonance
Imaging-Monitored Therapy[J] Circulation 2004; 110;2336-2341.
[31]毛焕元心脏病学／毛焕元主编.-2版.-北京：人民卫生出版社,20001017页。
[32]Yasushi Ishigaki, Hideki Katagiri et al. Impact of Plasma Oxidized Low-Density Lipoprotein Removal on Atherosclerosis[J] Circulation 2008;118;75-83.
[33]Tillmann Cyrus Yuemang Yao et al. Vitamin E Reduces Progression of Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient Mice With Established Vascular Lesions[J] Circulation 2003;107;521-523.
[34]Syed Husain, Neil P. Andrews et al. Aspirin Improves Endothelial Dysfunction in Atherosclerosis[J] Circulation 1998;97;716-720.
[35]中国高血压防治指南修订委员会中国高血压防治指南(2005年修订版全文)2005.
[36]Linda Brookes, MSc ESH'07:New Consensus Hypertension Guidelines From the European Society of Hypertension/European Society of Cardiology (ESH/ESC) 2007.
[37]胡高文,程晓昱 中医药防治动脉粥样硬化的研究进展[J]中西医结合心脑血管病杂志2009年2月第7巷第2期.