剪切力增高对大鼠腹主动脉管径及管壁MMP-9表达的影响
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摘要
目的：观察腹主动脉局部动脉壁剪切力增高对腹主动脉管径及管壁MMP-9表达的影响，并分析剪切力增高在动脉重塑中的作用。
方法：S-D大鼠48只，随机分8组，每组6只，4组为实验组，4组为对照组。实验组行肾动脉下腹主动脉-下腔静脉细针穿刺造瘘，对照组除不造瘘外，各项操作同实验组。分别于术后1天，7天，14天，28天取标本，并分别在术后即时和取标本时测瘘口近端动脉外径，免疫组化及IPP图像分析技术观察MMP-9动态表达及瘘口近端动脉内径周长，管壁厚度的改变。
结果：术后即时，瘘口近端动脉管径稍有扩张，但与术前无明显差异，术后第1天，瘘口近端动脉管径明显增大(P＜0.05)，扩张率达19％，管壁变薄(P＜0.05)，并随时间增加，管径不断增大，管壁不断变薄，到术后28天，动脉管径几乎达到未造瘘时的2倍；部分动脉扭曲明显；内皮细胞结构逐渐紊乱，内弹力层崩解，管壁大量炎性细胞浸润，中膜平滑肌结构进行性紊乱；MMP-9于术后1天开始表达，术后7天达高峰(P＜0.01)，并持续高表达(P＜0.01)。
结论：1．剪切力增高可使局部动脉出现管径增大，管壁变薄的正性重塑；2．剪切力增高导致管壁MMP-9表达上调；3．动脉管径增大及管壁变薄与MMP-9表达增高密切相关；4．剪切力增高，MMP-9表达增多是导致动脉瘤形成后逐渐增大及动静脉瘘形成后瘘口近远端逐渐膨大的主要因素。
Objective: To observe the expression of MMP-9 and the arterial caliber change in conditions that local arterial wall sheer stress is elevated and analyse the relationship between high shear stress and arterial remodling.
Methods: 48 S-D rats were divided into 4 experiment and 4 comparison groups averagely at radom, During the operation of the experiment groups, An infra-renal aortocaval fistula was construsted by needle puncture using a 22-G needle.The aorta proximal to the fistula was harvested after 1 day,7 days, 14 days and 28 days respectively,while sham operations were done in the comparison groups.The diameters of the aorta were measured after fistula made and before harvest.The internal perimeter and wall thickness were measured by computer skills.The level change of MMP-9 was observed by immunohistochemistry and computer skills.
Results: The diameters and the internal perimeters were enlarged in the 1day group at the sacrifice time (p<0.05),and the value was growing with the time ;Meanwhile, wall thickness were decreased with the time. Large amount of inflammatory cells soakaged the hemal wall,and endothelial cells and internal elastic lamina were destructed with the time,Stastics of all the result showed that MMP-9 had reached the peak value in the 7days group(p<0.01) ,and remained a high level expression continually.
Conclusions: when shear stress increases, the diameters of arteries increase by company of wall thickness decrease; the expression of MMP-9 up-regulates and gets a top in 7 day after operation ;the enlargement of the aorta and the decrease of wall thickness has a close relationship with the continuous expression of the MMP-9;and MMP-9 may be involved in the flow induced arterial remodling.
方法：S-D大鼠48只，随机分8组，每组6只，4组为实验组，4组为对照组。实验组行肾动脉下腹主动脉-下腔静脉细针穿刺造瘘，对照组除不造瘘外，各项操作同实验组。分别于术后1天，7天，14天，28天取标本，并分别在术后即时和取标本时测瘘口近端动脉外径，免疫组化及IPP图像分析技术观察MMP-9动态表达及瘘口近端动脉内径周长，管壁厚度的改变。
结果：术后即时，瘘口近端动脉管径稍有扩张，但与术前无明显差异，术后第1天，瘘口近端动脉管径明显增大(P＜0.05)，扩张率达19％，管壁变薄(P＜0.05)，并随时间增加，管径不断增大，管壁不断变薄，到术后28天，动脉管径几乎达到未造瘘时的2倍；部分动脉扭曲明显；内皮细胞结构逐渐紊乱，内弹力层崩解，管壁大量炎性细胞浸润，中膜平滑肌结构进行性紊乱；MMP-9于术后1天开始表达，术后7天达高峰(P＜0.01)，并持续高表达(P＜0.01)。
结论：1．剪切力增高可使局部动脉出现管径增大，管壁变薄的正性重塑；2．剪切力增高导致管壁MMP-9表达上调；3．动脉管径增大及管壁变薄与MMP-9表达增高密切相关；4．剪切力增高，MMP-9表达增多是导致动脉瘤形成后逐渐增大及动静脉瘘形成后瘘口近远端逐渐膨大的主要因素。
Objective: To observe the expression of MMP-9 and the arterial caliber change in conditions that local arterial wall sheer stress is elevated and analyse the relationship between high shear stress and arterial remodling.
Methods: 48 S-D rats were divided into 4 experiment and 4 comparison groups averagely at radom, During the operation of the experiment groups, An infra-renal aortocaval fistula was construsted by needle puncture using a 22-G needle.The aorta proximal to the fistula was harvested after 1 day,7 days, 14 days and 28 days respectively,while sham operations were done in the comparison groups.The diameters of the aorta were measured after fistula made and before harvest.The internal perimeter and wall thickness were measured by computer skills.The level change of MMP-9 was observed by immunohistochemistry and computer skills.
Results: The diameters and the internal perimeters were enlarged in the 1day group at the sacrifice time (p<0.05),and the value was growing with the time ;Meanwhile, wall thickness were decreased with the time. Large amount of inflammatory cells soakaged the hemal wall,and endothelial cells and internal elastic lamina were destructed with the time,Stastics of all the result showed that MMP-9 had reached the peak value in the 7days group(p<0.01) ,and remained a high level expression continually.
Conclusions: when shear stress increases, the diameters of arteries increase by company of wall thickness decrease; the expression of MMP-9 up-regulates and gets a top in 7 day after operation ;the enlargement of the aorta and the decrease of wall thickness has a close relationship with the continuous expression of the MMP-9;and MMP-9 may be involved in the flow induced arterial remodling.
引文
[1]. Raul J Guzman, Andrew Krystkowiak, Christopher K Zarins. Early and Sustained Medial Cell Activation after Aortocaval FistulaCreation in Mice. Journal of Surgical Research, 2002, 108, 112-121
[2]. Eiketsu Sho, Mien Sho, Hiroshi Nanjo, Koichi Kawamura. Hemodynamic Regulation of CD34~+ Cell Localization and Differentiation in Experimental Aneurysms. Arterioscler. Thromb. Vasc Biol. 2004, 24; 1916-1921
[3]. Takeshi K, Nakahashi, Katsuyuki Hoshina, Philip S Tsao, Eiketsu Sho. Flow Loading Induces Macrophage Antioxidative Gene Expression in Experimental Aneurysms Arterioscler. Thromb. Vasc Biol. 2002; 22; 2017-2022
[4]. Chengpei Xu, Sheila Lee, Chang Shu, Hirotake Masuda and Christopher K, Zarins, Expression of TGF-β1 and β3 but not apoptosis factors relates to flow-induced aortic enlargement. BMC Cardiovascular Disorders. 2002, 2: 11
[5]. Gibbons GH, Dzau VJ. The emerging concept of vascular remodeling. The New England Journal of Medicine, 1994, 330 (20): 1431-1438.
[6]. Silver, Annemarie E, Vita, Joseph A. Shear Stress-Mediated Arterial Remodeling in Atherosclerosis: Too Much of a Good Thing? Circulation. 2006, 113(24): 2787-2789
[7]. Castier, Yves, Brandes, Ralf P, Leseche, Guy, Tedgui, Alain, Lehoux, Stephanie p47phox-Dependent NADPH Oxidase Regulates Flow-Induced Vascular Remodeling. Circulation Research. 2005, 97(6): 533-540
[8]. Sho, Eiketsu, Nanjo, Hiroshi, Sho, Mien, Takahashi, Masato, Sugita, Akihiro, Kobayashi, Mikio, Kawamura, Koichi, Hirotake. P51 Early Activation of Endothelial Cells in Response to High Flow Regulates Carotid Arterial Remodeling. Arteriosclerosis, Thrombosis & Vascular Biology. 2004, 24(5): E-10
[9]. Yasmin, Wallace, Sharon, McEniery, Carmel M, Dakham, Zahid, Pusalkar, Pawan, Maki-Petaja, Matrix Metalloproteinase-9 (MMP-9), MMP-2, and Serum Elastase Activity Are Associated With Systolic Hypertension and Arterial Stiffness. Arteriosclerosis, Thrombosis & Vascular Biology. 2005, 25(2): 372-378
[10]. Saito S, Zempo N, Yamashita A, Takenaka H, et al. Matrx metalloproteinase expressions in arteriosclerotic aneurysmal diseas. Vasc Endovascular Surg, 2002, 36(1): 1-7
[11]. Newby, Andrew C. Do metalloproteinases destabilize vulnerable atherosclerotic plaques?. Current Opinion in Lipidology. 2006, 17(5): 556-561
[12]. Jahanning JM, Armstrong PJ, Franklin DP. et a f. Nitric oxide in experimental aneurysm form ation. early events and consequences of Nitric oxide inhibition. Ann Vasc Surg. 2002, 16(1): 65-72.
[13]. Dumont, Odile, Loufrani, Laurent Henrion, Daniel. Key Role of the NO-Pathway and Matrix Metalloprotease-9 in High Blood Flow-Induced Remodeling of Rat Resistance Arteries. Arteriosclerosis, Thrombosis & Vascular Biology. 2007, 27(2): 317-324
[14]. Wight, Thomas N. The ADAMTS Proteases, Extracellular Matrix, and Vascular Disease: Waking the Sleeping Giant(s)! Arteriosclerosis, Thrombosis & Vascular Biology. 2005, 25(1): 12-14
[15]. Prior, Barry M, Lloyd, Pamela G., Yang, H. T; Terjung, Ronald L. Exercise-Induced Vascular Remodeling. Exercise & Sport Sciences Reviews. 2003, 31(1): 26-33
[16]. Tomasian D , Keaney JF, Vita JA. Antioxidants and the bioactivity of endotheli-um-derived nitric oxide. Cardiovasc Res, 2000, 47(3): 426-435
[17]. Leung J, Wright A, Cheshire N, Thom SA, Hughes AD, Xu XY. Flow pattern and wall shear stresses in patient-specific models of the abdominal aortic aneurysm. Stud Health Technol Inform. 2004; 103: 235-238
[1]. Yao, Xiaoqiang, Garland, Christopher J. Recent Developments in Vascular Endothelial Cell Transient Receptor Potential Channels. Circulation Research. 2005, 97(9): 853-863
[2]. Heagerty AM, Aalkjer C, Bund SJ, et al. Small artery structure in hypertension: dual processes of growth.. Hypertension, 1993, 21 (4): 391-397.
[3]. Gibbons GH, Dzau VJ. The emerging concept of vascular remodeling.. The New England Journal of Medicine, 1994, 330 (20): 1431-1438.
[4]. ZHANG Li-fan, YU Zhi-bin, MA Jin, et al. Peripheral effector mechanism hypothesis on cardiovascular dysfunction after spaceflight. Progress in Physiological Sciences, 2001, 32(1): 13-17
[5]. Langille BL. Remodeling of developing and mature arteries: endothelium, smooth muscle, and matrix. J Cadiovasc Pharmacol, 1993, 21 (sl): 11-17.
[6]. Kawamura K, Murakami M, Zarins CK, Adaptive remodeling of internal elastic lamina and endothelial lining during flow-induced arterial enlargement. Thromb. Vasc. Biol. 2002; 22
[7]. Sasaki T, Zhuang YJ, Masuda H, Zarins CK. Basic fibroblast growth factor expression precedes flow-induced arterial enlargement, Arteriosclerosis, Thrombosis &Vascular Biology. 2004, 24(5): E-10
[8]. Raul J. Guzman, Andrew Krystkowiak, Christopher K. Zarins, Early and Sustained Medial Cell Activation after Aortocaval Fistula Creation in Mice. Journal of Surgical Research2002, 108, 112-121
[9]. Eiketsu Sho, Mien Sho, Hiroshi Nanjo, Koichi Kawamura, Hemodynamic Regulation of CD34+ Cell Localization and Differentiation in Experimental Aneurysms. Arterioscler. Thromb. Vasc. Biol. 2004; 24; 1916-1921;
[10]. Platt, Manu O, Ankeny, Randall F, Jo, Hanjoong Laminar Shear Stress Inhibits Cathepsin L Activity in Endothelial Cells. Arteriosclerosis, Thrombosis & Vascular Biology. 2006, 26(8): 1784-1790
[11]. Dull RO, Mechanism of flow mediated signal transduction in endothelial cells: kinetics of ATP surface concentration. J Vasc Res, 1999, 29(6): 410-419.
[12]. Davies PF. Endothelium as a signal tranduction interface for flow force: cell surface dynamics. Thromb Haemost, 1993, 70(1): 124-128
[13]. Malek AM. Role of tyrosine, intracellular calcium release, and mechanosensitive channels in endothelial shear stress transduction. Circulation, 1993; 88 (3)
[14]. Tzima E, Del Pozo MA, Shattil S J, et al. Activation of integrins in endothelial cells by fluid shear stress mediates Rhodependent cytoskeletal alignment. EMBO J, 2001, 20: 4
[15]. CHEN Youqing, CHEN Huaiqing. The influence of different types of shear stress on physiology and biochemistry of vascular endothelial cells. Foreign Medical Sciences—Biomedical Engineering Fascicle, 2000, 23 (4): 233-238.
[16]．刘乃奎，唐朝枢。血管重塑的细胞与分子生物学[M]。北京：北京医科大学出版社，1999．303-305
[17] Simionescu, Maya Implications of Early Structural-Functional Changes in the Endothelium for Vascular Disease. Arteriosclerosis, Thrombosis & Vascular Biology. 2007, 27(2): 266-274
[18] Cheng, Caroline, Tempel, Dennie BSc, van Haperen, Rien BSc; van der Baan, Arjen BSc, Grosveld, Atherosclerotic Lesion Size and Vulnerability Are Determined by Patterns of Fluid Shear Stress. Circulation. 2006, 113(23): 2744-2753
[19]. Pasterkamp, Gerard, Galis, Zorina S, de Kleijn, Dominique P. V. Expansive Arterial Remodeling: Location, Location, Location. Arteriosclerosis, Thrombosis & Vascular Biology. 2004, 24(4): 650-657
[20]. Jahanning JM, Armstrong PJ, Franklin DP. et al. Nitric oxide in experimental anemysm form ation: early events and consequences of Nitric oxide inhibition. Ann Vasc Surg. 2002, 16(1): 65-72.
[21]. Hashimoto, Tomoki MD, Matsumoto, Melissa M BS, Tsang, Eric J BS, Young, William L MD. Critical roles of neutrophils and macrophages in flow-induced adaptive outward vascular remodeling. Journal of Neurosurgical Anesthesiology. 2006,18(4):293
[22]. sho, Eiketsu, Sho, Mien, Singh, Tej M, Xu, Chengpei, Zarins, Christopher K, Masuda, Hirotake Blood Flow Decrease Induces Apoptosis of Endothelial Cells in Previously Dilated Arteries Resulting From Chronic High Blood Flow. Arteriosclerosis, Thrombosis & Vascular Biology. 2001,21 (7): 1139-1145
[23]. F isher AB, Ch ien S, Barakat A I, et al. Endo thelial cellular response to altered shear stress[J]. A m J Physiol Lung Cell M ol Physiol, 2001, 281 (3): L 529
[24]. Shiran A, Mintz GS, Leiboff B, Kent KM, Pichard AD, Satler LF, et al.Serial volumetric intravascular ultrasound assessment of arterial remodeling in left main coronary artery disease. Am J Cardiol, 1999,83 (10): 427-432
[25]. Mayr M, Xu Q. Smooth muscle cell apoptosis in arteriosclerosis. Exp Gerontol, 2001,36 (7): 969-987
[26]. Kockx MM, Herman AG. Apoptosis in atherosclerosis: beneficial or detrimental? Cardiovasc Res, 2000,45 (3): 736-746
[27]. L um RM, Wiley LM, Barakat A I, et al. Influence of different forms of fluid shear stress on vascular endo thelial TGF-betal mRNA exp ression[J]. Int J M olM ed, 2000, 5 (6): 635-641
[28]. Chengpei Xu, Sheila Lee, Chang Shu, Hirotake Masuda and Christopher K,Zarins,Expression of TGF-β1 and β3 but not apoptosis factors relates to flow-induced aortic enlargement.BMC Cardiovascular Disorders 2002, 2:11
[29]. Molavi, Behzad; Mehta, Jawahar L. Oxidative stress in cardiovascular disease: molecular basis of its deleterious effects, its detection, and therapeutic considerations. Current Opinion in Cardiology. 2004,19(5):488-493
[30]. Go sgnachW, ChallahM, Coulet F, et al. Shear stress induces angiotensin converting enzyme expression in cultured smooth muscle cells: po ssible invo lvement of bFGF. Card iovasc Res, 2000, 45 (2): 486-492.
[31]. Masuda, Hirotake, Zhuang, Yong-Jie, Singh, Tej M, Kawamura, Koichi, Murakami, Masayo, Zarins, Christopher K, Glagov, Seymour Adaptive Remodeling of Internal Elastic Lamina and Endothelial Lining During Flow-Induced Arterial Enlargement. Arteriosclerosis, Thrombosis & Vascular Biology. 1999, 19(10): 2298-2307
[32]. SU Hai2xia, SHENGJing. Study progress in the phenotypic ofsmooth muscle cells in vessel after injure. Foreign Medical Sciences Section of Cardiovascular Disease, 2002, 29 (1): 10-12
[33]. N athalie B, Karillon GJ, M erval R, et al. Differential effects of pressure and flow on DNA and p ro tein synthesis and on fibronectin expression by arteries and a novel organ culture system. Circ Res, 2005, 77 (2): 684
[34]. Tronc, F, Mallat, Z, Lehoux, S, Wasset, M, Tedgui, A. Role of MMPs in Blood Flow-Induced Vascular Remodeling. Hypertension. 1998, 32(4): 805
[35]. Yasmin, Wallace, Sharon, McEniery, Carmel M, Dakham, Zahid; Pusalkar, Pawan, Maki-Petaja, Matrix Metalloproteinase-9 (MMP-9), MMP-2, and Serum Elastase Activity Are Associated With Systolic Hypertension and Arterial Stiffness. Arteriosclerosis, Thrombosis & Vascular Biology. 2005, 25(2): 372-378
[36]. Saito S, Zempo N, Yamashita A, Takenaka H, et al. Matrx metalloproteinase expressions in arteriosclerotic aneurysmal disease. Vasc Endovascular Surg, 2002, 36(1): 1-7
[37]. Spinale FG, Coker ML, Bond BR, et al. Myocardialmatrix degradation and matelloproteinase activation in the failing heart: a potential therapeutic target Cardiovasc Res, 2000, 46(2): 225-238.
[38]. Eiketsu Sho, Mien Sho, Hiroshi Nanjo, Koichi Kawamura, Hemodynamic Regulation of CD34 Cell Localization and Differentiation in Experimental Aneurysms. Arterioscler. Thromb. Vasc. Biol. 2004; 24; 1916-1921;
[39]. Takeshi K. Nakahashi, Katsuyuki Hoshina, Philip S. Tsao, Eiketsu Sho, Mien Sho, Flow Loading Induces Macrophage Antioxidative Gene Expression in Experimental Aneurysms Arterioscler. Thromb. Vasc. Biol. 2002; 22; 2017-2022;
[40] Taniyama, Yoshihiro, Griendling, Kathy K. Reactive Oxygen Species in the Vasculature: Molecular and Cellular Mechanisms. Hypertension. 2003, 42(6): 1075-1081
[2]. Eiketsu Sho, Mien Sho, Hiroshi Nanjo, Koichi Kawamura. Hemodynamic Regulation of CD34~+ Cell Localization and Differentiation in Experimental Aneurysms. Arterioscler. Thromb. Vasc Biol. 2004, 24; 1916-1921
[3]. Takeshi K, Nakahashi, Katsuyuki Hoshina, Philip S Tsao, Eiketsu Sho. Flow Loading Induces Macrophage Antioxidative Gene Expression in Experimental Aneurysms Arterioscler. Thromb. Vasc Biol. 2002; 22; 2017-2022
[4]. Chengpei Xu, Sheila Lee, Chang Shu, Hirotake Masuda and Christopher K, Zarins, Expression of TGF-β1 and β3 but not apoptosis factors relates to flow-induced aortic enlargement. BMC Cardiovascular Disorders. 2002, 2: 11
[5]. Gibbons GH, Dzau VJ. The emerging concept of vascular remodeling. The New England Journal of Medicine, 1994, 330 (20): 1431-1438.
[6]. Silver, Annemarie E, Vita, Joseph A. Shear Stress-Mediated Arterial Remodeling in Atherosclerosis: Too Much of a Good Thing? Circulation. 2006, 113(24): 2787-2789
[7]. Castier, Yves, Brandes, Ralf P, Leseche, Guy, Tedgui, Alain, Lehoux, Stephanie p47phox-Dependent NADPH Oxidase Regulates Flow-Induced Vascular Remodeling. Circulation Research. 2005, 97(6): 533-540
[8]. Sho, Eiketsu, Nanjo, Hiroshi, Sho, Mien, Takahashi, Masato, Sugita, Akihiro, Kobayashi, Mikio, Kawamura, Koichi, Hirotake. P51 Early Activation of Endothelial Cells in Response to High Flow Regulates Carotid Arterial Remodeling. Arteriosclerosis, Thrombosis & Vascular Biology. 2004, 24(5): E-10
[9]. Yasmin, Wallace, Sharon, McEniery, Carmel M, Dakham, Zahid, Pusalkar, Pawan, Maki-Petaja, Matrix Metalloproteinase-9 (MMP-9), MMP-2, and Serum Elastase Activity Are Associated With Systolic Hypertension and Arterial Stiffness. Arteriosclerosis, Thrombosis & Vascular Biology. 2005, 25(2): 372-378
[10]. Saito S, Zempo N, Yamashita A, Takenaka H, et al. Matrx metalloproteinase expressions in arteriosclerotic aneurysmal diseas. Vasc Endovascular Surg, 2002, 36(1): 1-7
[11]. Newby, Andrew C. Do metalloproteinases destabilize vulnerable atherosclerotic plaques?. Current Opinion in Lipidology. 2006, 17(5): 556-561
[12]. Jahanning JM, Armstrong PJ, Franklin DP. et a f. Nitric oxide in experimental aneurysm form ation. early events and consequences of Nitric oxide inhibition. Ann Vasc Surg. 2002, 16(1): 65-72.
[13]. Dumont, Odile, Loufrani, Laurent Henrion, Daniel. Key Role of the NO-Pathway and Matrix Metalloprotease-9 in High Blood Flow-Induced Remodeling of Rat Resistance Arteries. Arteriosclerosis, Thrombosis & Vascular Biology. 2007, 27(2): 317-324
[14]. Wight, Thomas N. The ADAMTS Proteases, Extracellular Matrix, and Vascular Disease: Waking the Sleeping Giant(s)! Arteriosclerosis, Thrombosis & Vascular Biology. 2005, 25(1): 12-14
[15]. Prior, Barry M, Lloyd, Pamela G., Yang, H. T; Terjung, Ronald L. Exercise-Induced Vascular Remodeling. Exercise & Sport Sciences Reviews. 2003, 31(1): 26-33
[16]. Tomasian D , Keaney JF, Vita JA. Antioxidants and the bioactivity of endotheli-um-derived nitric oxide. Cardiovasc Res, 2000, 47(3): 426-435
[17]. Leung J, Wright A, Cheshire N, Thom SA, Hughes AD, Xu XY. Flow pattern and wall shear stresses in patient-specific models of the abdominal aortic aneurysm. Stud Health Technol Inform. 2004; 103: 235-238
[1]. Yao, Xiaoqiang, Garland, Christopher J. Recent Developments in Vascular Endothelial Cell Transient Receptor Potential Channels. Circulation Research. 2005, 97(9): 853-863
[2]. Heagerty AM, Aalkjer C, Bund SJ, et al. Small artery structure in hypertension: dual processes of growth.. Hypertension, 1993, 21 (4): 391-397.
[3]. Gibbons GH, Dzau VJ. The emerging concept of vascular remodeling.. The New England Journal of Medicine, 1994, 330 (20): 1431-1438.
[4]. ZHANG Li-fan, YU Zhi-bin, MA Jin, et al. Peripheral effector mechanism hypothesis on cardiovascular dysfunction after spaceflight. Progress in Physiological Sciences, 2001, 32(1): 13-17
[5]. Langille BL. Remodeling of developing and mature arteries: endothelium, smooth muscle, and matrix. J Cadiovasc Pharmacol, 1993, 21 (sl): 11-17.
[6]. Kawamura K, Murakami M, Zarins CK, Adaptive remodeling of internal elastic lamina and endothelial lining during flow-induced arterial enlargement. Thromb. Vasc. Biol. 2002; 22
[7]. Sasaki T, Zhuang YJ, Masuda H, Zarins CK. Basic fibroblast growth factor expression precedes flow-induced arterial enlargement, Arteriosclerosis, Thrombosis &Vascular Biology. 2004, 24(5): E-10
[8]. Raul J. Guzman, Andrew Krystkowiak, Christopher K. Zarins, Early and Sustained Medial Cell Activation after Aortocaval Fistula Creation in Mice. Journal of Surgical Research2002, 108, 112-121
[9]. Eiketsu Sho, Mien Sho, Hiroshi Nanjo, Koichi Kawamura, Hemodynamic Regulation of CD34+ Cell Localization and Differentiation in Experimental Aneurysms. Arterioscler. Thromb. Vasc. Biol. 2004; 24; 1916-1921;
[10]. Platt, Manu O, Ankeny, Randall F, Jo, Hanjoong Laminar Shear Stress Inhibits Cathepsin L Activity in Endothelial Cells. Arteriosclerosis, Thrombosis & Vascular Biology. 2006, 26(8): 1784-1790
[11]. Dull RO, Mechanism of flow mediated signal transduction in endothelial cells: kinetics of ATP surface concentration. J Vasc Res, 1999, 29(6): 410-419.
[12]. Davies PF. Endothelium as a signal tranduction interface for flow force: cell surface dynamics. Thromb Haemost, 1993, 70(1): 124-128
[13]. Malek AM. Role of tyrosine, intracellular calcium release, and mechanosensitive channels in endothelial shear stress transduction. Circulation, 1993; 88 (3)
[14]. Tzima E, Del Pozo MA, Shattil S J, et al. Activation of integrins in endothelial cells by fluid shear stress mediates Rhodependent cytoskeletal alignment. EMBO J, 2001, 20: 4
[15]. CHEN Youqing, CHEN Huaiqing. The influence of different types of shear stress on physiology and biochemistry of vascular endothelial cells. Foreign Medical Sciences—Biomedical Engineering Fascicle, 2000, 23 (4): 233-238.
[16]．刘乃奎，唐朝枢。血管重塑的细胞与分子生物学[M]。北京：北京医科大学出版社，1999．303-305
[17] Simionescu, Maya Implications of Early Structural-Functional Changes in the Endothelium for Vascular Disease. Arteriosclerosis, Thrombosis & Vascular Biology. 2007, 27(2): 266-274
[18] Cheng, Caroline, Tempel, Dennie BSc, van Haperen, Rien BSc; van der Baan, Arjen BSc, Grosveld, Atherosclerotic Lesion Size and Vulnerability Are Determined by Patterns of Fluid Shear Stress. Circulation. 2006, 113(23): 2744-2753
[19]. Pasterkamp, Gerard, Galis, Zorina S, de Kleijn, Dominique P. V. Expansive Arterial Remodeling: Location, Location, Location. Arteriosclerosis, Thrombosis & Vascular Biology. 2004, 24(4): 650-657
[20]. Jahanning JM, Armstrong PJ, Franklin DP. et al. Nitric oxide in experimental anemysm form ation: early events and consequences of Nitric oxide inhibition. Ann Vasc Surg. 2002, 16(1): 65-72.
[21]. Hashimoto, Tomoki MD, Matsumoto, Melissa M BS, Tsang, Eric J BS, Young, William L MD. Critical roles of neutrophils and macrophages in flow-induced adaptive outward vascular remodeling. Journal of Neurosurgical Anesthesiology. 2006,18(4):293
[22]. sho, Eiketsu, Sho, Mien, Singh, Tej M, Xu, Chengpei, Zarins, Christopher K, Masuda, Hirotake Blood Flow Decrease Induces Apoptosis of Endothelial Cells in Previously Dilated Arteries Resulting From Chronic High Blood Flow. Arteriosclerosis, Thrombosis & Vascular Biology. 2001,21 (7): 1139-1145
[23]. F isher AB, Ch ien S, Barakat A I, et al. Endo thelial cellular response to altered shear stress[J]. A m J Physiol Lung Cell M ol Physiol, 2001, 281 (3): L 529
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