两种血流动力学状态下大鼠动脉血管反应性变化及其机理的研究
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摘要
心血管疾病目前是世界上发病率和死亡率最高的疾患之一。血流动力学状态的变化对血管结构和功能有着重要的影响。诸如动脉粥样硬化、血栓形成、心肌梗死、高血压、冠心病等常见心血管疾病的发生都与动脉血管中的血液流动密切相关。血液流动区域内压力、速度、管壁切应力的变化,可以通过影响动脉血管平滑肌细胞和内皮细胞的适应性机制,导致血管壁发生病理改变。甲状腺功能亢进会造成动脉血管血液流动区域内的压力增高、速度加快、管壁切应力变大;模拟失重将导致冠状动脉系统灌注压下降,血流减少,血液流动区域内的压力下降、速度减慢、管壁切应力变小。这两种高、低不同的血流动力学状态与心血管疾病的关系还缺乏深入系统的研究。因此可以通过深入研究不同血流动力学状态对动脉血管的影响,来更好地了解心血管疾病的发病机理。
目的通过研究甲状腺功能亢时动脉内血液流动的高动力状态及模拟失重时冠状动脉内血液流动的低动力状态对血管反应性的影响,了解心血管疾病的发病机理及航天飞行后立位耐力不良的发生机理。方法建立甲亢大鼠模型及尾部悬吊模拟失重大鼠模型。采用离体动脉血管环技术研究甲亢大鼠肾动脉、肠系膜动脉、股动脉、颈总动脉和脑基底动脉、肠系膜分支小动脉血管反应性的改变,以及模拟失重大鼠冠状动脉血管反应性的改变;利用光镜、电镜技术对模拟失重大鼠冠状动脉组织形态及超微结构的改变进行观察;利用蛋白免疫印迹技术测定动脉中eNOS和iNOS蛋白表达。
结果
1、甲亢时高血流动力学状态下,大鼠肾动脉、肠系膜动脉、股动脉、颈总动脉对KCl和PE的收缩反应性降低,对ACh的舒张反应性增强,对SNP的舒张反应无明显改变。甲亢大鼠各部位动脉对KCl、ACh敏感性增加,对PE、SNP敏感性没有明显改变。
2、甲亢时高血流动力学状态下,大鼠脑基底动脉、肠系膜分支小动脉血管对KCl和5-HT或PE的的收缩反应性降低,对ACh的舒张反应性增强,对SNP的舒张反应无明显改变。甲亢大鼠各部位小动脉对KCl、ACh敏感性增加,对5-HT或PE、SNP的敏感性没有明显改变。
3、甲亢大鼠肠系膜分支小动脉和基底动脉中eNOS蛋白表达量显著增多;甲亢大鼠肠系膜分支小动脉和基底动脉中检测到iNOS蛋白表达,而对照组中未检测到iNOS蛋白表达。
4、两周模拟失重大鼠冠状动脉对KCl和PE的收缩反应性降低,对ACh、SNP的舒张反应性降低;对KCl、ACh的敏感性下降,对PE、SNP敏感性没有明显改变。
5、两周模拟失重大鼠冠状动脉组织形态及超微结构观察发现,血管平滑肌萎缩,血管内皮细胞发生病理改变。
6、两周模拟失重大鼠冠状动脉中eNOS蛋白表达显著降低;在模拟失重组及对照组大鼠冠状动脉中均未检测到iNOS蛋白表达。
结论甲亢时高血流动力学状态可能通过对血管平滑肌细胞及内皮细胞的影响,使动脉血管收缩反应性减弱、内皮依赖的舒张反应性增强;高血流动力学状态可能通过NO的增加,来使高切应力下血管的内皮依赖性舒张增强。模拟失重大鼠冠状动脉低血流动力学状态对冠状动脉产生了显著影响,冠状动脉收缩及舒张反应性均减弱,血管内皮细胞和血管平滑肌结构和功能发生病理改变,此变化在航天飞行后立位耐力不良及其他心血管疾病的发生机制中可能具有重要作用。
Cardiovascular disease is one of the most challening diseases in modernworld.The change of haemodynamic states significantly affects arterial structureand function.The hemokinesis in artery has great relationship with pathogenesis ofcardiovascular disease,such as artherosclerosis, thrombogenesis, heart infarction,hypertension and coronary artery disease.Alterations of pressure, velocity, andshear stress in artery result in pathological change of vessel wall,throughinfluencing adaptable mechanism of vascular smooth muscle cell and endothelialcell.Hyperthyroidism causes increased pressure,high speed and big shear stresswithin the arterial blood flow region.Whereas simulated weightlessness leadscoronary system to low perfusion pressure, reducing blood flow, therefore withinthe coronary arterial blood flow region it causes decreased pressure,low speed andsmall shear stress. But there is no in-depth and systematic research about therelationship between these high or low haemodynamic states and cardiovasculardisease.So we can get a better understanding of cardiovascular diseasepathogenesis through in-depth and systematic study of alterations in arterialreactivity under different haemodynamic states.
AIMAIMS Through studying alterations in arterial reactivity of various arteriesin rats under hingh haemodynamic state of hyperthyroidism and lowhaemodynamic state of simulated weightlessness,to understand the pathogenesisof cardiovascular disease and the mechanism of orthostatic intolerance after spaceflight.
METHODS Established hyperthyroid rat model and simulated weightlessnessrat model. By means of isolated arteries ring technology,studied alterations inarterial reactivity of renal artery,mesenteric artery,femoral artery,carotidartery,basilar artery, small mesenteric branches artery in hyperthyroid rats andcoronary artery in simulated weightlessness rats. Using light microscopy andelectron microscopy,observed morphology and ultrastructure changes of coronaryartery of simulated weightlessness rats.The eNOS and iNOS protein expressionswere observed by Western Blot technique.
RESULTS
1、The isometric contractile tensions evoked by KCl（10～100 mmol/L）andphenylephrine (PE) (10-9～10-4 mol/L)were significantly lower in renalarterial,mesenteric arterial,femoral arterial,carotid arterial rings from hyperthyroidrats compared with those of control ones (P<0.05). The vasodilator responseinduced by acetylcholine (ACh) (10-9～10-4 mol/L)was significantly increased inhyperthyroid group (P<0.05). But the differences of responses of those arterialrings induced by sodium nitroprusside (SNP) (10-9～10-4 mol/L)between twogroups were nonsignificant. The sensitivities of those arterial rings to KCl andACh were significantly enhanced by hyperthyroidism (P<0.05), whereas thesensitivity to PE and SNP did not show any significant differences between twogroups.
2、The isometric contractile tensions evoked by KCl and 5-HT or PE weresignificantly lower in basilar and small mesenteric branch arterial rings fromhyperthyroid rats compared with those of control ones (P<0.05). The vasodilatorresponse induced by ACh was significantly increased in hyperthyroid group(P<0.05). But the differences of responses of those arterial rings induced bysodium SNP between two groups were nonsignificant. The sensitivities of thosearterial rings to KCl and ACh were significantly enhanced by hyperthyroidism(P<0.05), whereas the sensitivity to 5-HT or PE and SNP did not show anysignificant differences between two groups.
3、The eNOS protein expression increased in basilar and small mesentericbranch artery of hyperthyroid rats compared with those of control ones (P<0.05).The iNOS protein expression occured in hyperthyroid rats but didn’t occure incontrol ones.
4、The isometric contractile tensions evoked by KCl and PE weresignificantly lower in coronary arterial rings from two weeks simulatedweightlessness rats compared with those of control ones (P<0.05). The vasodilatorresponse induced by ACh and SNP were significantly decreased in simulatedweightlessness group (P<0.05).The sensitivities of those arterial rings to KCl andACh were significantly decreased by simulated weightlessness (P<0.05), whereasthe sensitivity to PE and SNP did not show any significant differences betweentwo groups..
5、Morphology and ultrastructure changes of coronary arteries of two weekssimulated weightlessness rats were observed: pathological changes took place invascular endothelial cells and vascular smooth muscle was atrophical.
6、The eNOS protein expression decreased in coronary arteries of two weeks simulated weightlessness rats compared with those of control ones (P<0.05). TheiNOS protein expression didn’t occure in two groups.
CONCLUSION The high haemodynamic state of hyperthyroidism maybethrough influencing adaptable mechanism of vascular smooth muscle cell andvascular endothelial cell caused arteriel vasoconstriction weaken and theendothelium-dependent vasodilator response increase.The vascular endotheliumdependentvasodilation increased under high haemodynamic state maybe bymeans of the enhancement of NO. The low haemodynamic state of simulatedweightlessness significantly affected coronary arterial structure and function.Thecoronary arterial vasoconstriction and vasodilator response both decreased, andpathological changes took place in vascular endothelial cells and vascular smoothmuscle cells.This change may paly a role in pathogenesis of cardiovasculardisease and the mechanism of orthostatic intolerance after space flight.
目的通过研究甲状腺功能亢时动脉内血液流动的高动力状态及模拟失重时冠状动脉内血液流动的低动力状态对血管反应性的影响,了解心血管疾病的发病机理及航天飞行后立位耐力不良的发生机理。方法建立甲亢大鼠模型及尾部悬吊模拟失重大鼠模型。采用离体动脉血管环技术研究甲亢大鼠肾动脉、肠系膜动脉、股动脉、颈总动脉和脑基底动脉、肠系膜分支小动脉血管反应性的改变,以及模拟失重大鼠冠状动脉血管反应性的改变;利用光镜、电镜技术对模拟失重大鼠冠状动脉组织形态及超微结构的改变进行观察;利用蛋白免疫印迹技术测定动脉中eNOS和iNOS蛋白表达。
结果
1、甲亢时高血流动力学状态下,大鼠肾动脉、肠系膜动脉、股动脉、颈总动脉对KCl和PE的收缩反应性降低,对ACh的舒张反应性增强,对SNP的舒张反应无明显改变。甲亢大鼠各部位动脉对KCl、ACh敏感性增加,对PE、SNP敏感性没有明显改变。
2、甲亢时高血流动力学状态下,大鼠脑基底动脉、肠系膜分支小动脉血管对KCl和5-HT或PE的的收缩反应性降低,对ACh的舒张反应性增强,对SNP的舒张反应无明显改变。甲亢大鼠各部位小动脉对KCl、ACh敏感性增加,对5-HT或PE、SNP的敏感性没有明显改变。
3、甲亢大鼠肠系膜分支小动脉和基底动脉中eNOS蛋白表达量显著增多;甲亢大鼠肠系膜分支小动脉和基底动脉中检测到iNOS蛋白表达,而对照组中未检测到iNOS蛋白表达。
4、两周模拟失重大鼠冠状动脉对KCl和PE的收缩反应性降低,对ACh、SNP的舒张反应性降低;对KCl、ACh的敏感性下降,对PE、SNP敏感性没有明显改变。
5、两周模拟失重大鼠冠状动脉组织形态及超微结构观察发现,血管平滑肌萎缩,血管内皮细胞发生病理改变。
6、两周模拟失重大鼠冠状动脉中eNOS蛋白表达显著降低;在模拟失重组及对照组大鼠冠状动脉中均未检测到iNOS蛋白表达。
结论甲亢时高血流动力学状态可能通过对血管平滑肌细胞及内皮细胞的影响,使动脉血管收缩反应性减弱、内皮依赖的舒张反应性增强;高血流动力学状态可能通过NO的增加,来使高切应力下血管的内皮依赖性舒张增强。模拟失重大鼠冠状动脉低血流动力学状态对冠状动脉产生了显著影响,冠状动脉收缩及舒张反应性均减弱,血管内皮细胞和血管平滑肌结构和功能发生病理改变,此变化在航天飞行后立位耐力不良及其他心血管疾病的发生机制中可能具有重要作用。
Cardiovascular disease is one of the most challening diseases in modernworld.The change of haemodynamic states significantly affects arterial structureand function.The hemokinesis in artery has great relationship with pathogenesis ofcardiovascular disease,such as artherosclerosis, thrombogenesis, heart infarction,hypertension and coronary artery disease.Alterations of pressure, velocity, andshear stress in artery result in pathological change of vessel wall,throughinfluencing adaptable mechanism of vascular smooth muscle cell and endothelialcell.Hyperthyroidism causes increased pressure,high speed and big shear stresswithin the arterial blood flow region.Whereas simulated weightlessness leadscoronary system to low perfusion pressure, reducing blood flow, therefore withinthe coronary arterial blood flow region it causes decreased pressure,low speed andsmall shear stress. But there is no in-depth and systematic research about therelationship between these high or low haemodynamic states and cardiovasculardisease.So we can get a better understanding of cardiovascular diseasepathogenesis through in-depth and systematic study of alterations in arterialreactivity under different haemodynamic states.
AIMAIMS Through studying alterations in arterial reactivity of various arteriesin rats under hingh haemodynamic state of hyperthyroidism and lowhaemodynamic state of simulated weightlessness,to understand the pathogenesisof cardiovascular disease and the mechanism of orthostatic intolerance after spaceflight.
METHODS Established hyperthyroid rat model and simulated weightlessnessrat model. By means of isolated arteries ring technology,studied alterations inarterial reactivity of renal artery,mesenteric artery,femoral artery,carotidartery,basilar artery, small mesenteric branches artery in hyperthyroid rats andcoronary artery in simulated weightlessness rats. Using light microscopy andelectron microscopy,observed morphology and ultrastructure changes of coronaryartery of simulated weightlessness rats.The eNOS and iNOS protein expressionswere observed by Western Blot technique.
RESULTS
1、The isometric contractile tensions evoked by KCl（10～100 mmol/L）andphenylephrine (PE) (10-9～10-4 mol/L)were significantly lower in renalarterial,mesenteric arterial,femoral arterial,carotid arterial rings from hyperthyroidrats compared with those of control ones (P<0.05). The vasodilator responseinduced by acetylcholine (ACh) (10-9～10-4 mol/L)was significantly increased inhyperthyroid group (P<0.05). But the differences of responses of those arterialrings induced by sodium nitroprusside (SNP) (10-9～10-4 mol/L)between twogroups were nonsignificant. The sensitivities of those arterial rings to KCl andACh were significantly enhanced by hyperthyroidism (P<0.05), whereas thesensitivity to PE and SNP did not show any significant differences between twogroups.
2、The isometric contractile tensions evoked by KCl and 5-HT or PE weresignificantly lower in basilar and small mesenteric branch arterial rings fromhyperthyroid rats compared with those of control ones (P<0.05). The vasodilatorresponse induced by ACh was significantly increased in hyperthyroid group(P<0.05). But the differences of responses of those arterial rings induced bysodium SNP between two groups were nonsignificant. The sensitivities of thosearterial rings to KCl and ACh were significantly enhanced by hyperthyroidism(P<0.05), whereas the sensitivity to 5-HT or PE and SNP did not show anysignificant differences between two groups.
3、The eNOS protein expression increased in basilar and small mesentericbranch artery of hyperthyroid rats compared with those of control ones (P<0.05).The iNOS protein expression occured in hyperthyroid rats but didn’t occure incontrol ones.
4、The isometric contractile tensions evoked by KCl and PE weresignificantly lower in coronary arterial rings from two weeks simulatedweightlessness rats compared with those of control ones (P<0.05). The vasodilatorresponse induced by ACh and SNP were significantly decreased in simulatedweightlessness group (P<0.05).The sensitivities of those arterial rings to KCl andACh were significantly decreased by simulated weightlessness (P<0.05), whereasthe sensitivity to PE and SNP did not show any significant differences betweentwo groups..
5、Morphology and ultrastructure changes of coronary arteries of two weekssimulated weightlessness rats were observed: pathological changes took place invascular endothelial cells and vascular smooth muscle was atrophical.
6、The eNOS protein expression decreased in coronary arteries of two weeks simulated weightlessness rats compared with those of control ones (P<0.05). TheiNOS protein expression didn’t occure in two groups.
CONCLUSION The high haemodynamic state of hyperthyroidism maybethrough influencing adaptable mechanism of vascular smooth muscle cell andvascular endothelial cell caused arteriel vasoconstriction weaken and theendothelium-dependent vasodilator response increase.The vascular endotheliumdependentvasodilation increased under high haemodynamic state maybe bymeans of the enhancement of NO. The low haemodynamic state of simulatedweightlessness significantly affected coronary arterial structure and function.Thecoronary arterial vasoconstriction and vasodilator response both decreased, andpathological changes took place in vascular endothelial cells and vascular smoothmuscle cells.This change may paly a role in pathogenesis of cardiovasculardisease and the mechanism of orthostatic intolerance after space flight.
引文
[1] Kivimaki M, Lawlor DA, Davey Smith G, Kouvonen A, Virtanen M, Elovainio M,VahteraJ. Socioeconomic position, co-occurrence of behavior-related risk factors, andcoronary heart disease: the Finnish Public Sector study. Am J Public Health, 2007,97(5):874-9.
[2] Grigioni M, Daniele C, D'Avenio G,Barbaro V. On the monodimensional approach tothe estimation of the highest reynolds shear stress in a turbulent flow. JBiomech, 2000, 33(6):701-8.
[3] Moore JA, Steinman DA,Ethier CR. Computational blood flow modelling: errorsassociated with reconstructing finite element models from magnetic resonanceimages. J Biomech, 1998, 31(2):179-84.
[4] Couteau B, Payan Y,Lavallee S. The mesh-matching algorithm: an automatic 3D meshgenerator for finite element structures. J Biomech, 2000, 33(8):1005-9.
[5] Cebral JR, Lohner R, Choyke PL,Yim PJ. Merging of intersecting triangulations forfinite element modeling. J Biomech, 2001, 34(6):815-9.
[6] Etave F, Finet G, Boivin M, Boyer JC, Rioufol G,Thollet G. Mechanical propertiesof coronary stents determined by using finite element analysis. J Biomech, 2001,34(8):1065-75.
[7] Malek AM, Alper SL,Izumo S. Hemodynamic shear stress and its role inatherosclerosis. JAMA, 1999, 282(21):2035-42.
[8] Rieder MJ, Carmona R, Krieger JE, Pritchard KA Jr,Greene AS. Suppression ofangiotensin-converting enzyme expression and activity by shear stress. Circ Res,1997, 80(3):312-9.
[9] Liu Y, Chen BP, Lu M, Zhu Y, Stemerman MB, Chien S,Shyy JY. Shear stressactivation of SREBP1 in endothelial cells is mediated by integrins. ArteriosclerThromb Vasc Biol, 2002, 22(1):76-81.
[10] Chen BP, Li YS, Zhao Y, Chen KD, Li S, Lao J, Yuan S, Shyy JY,Chien S. DNAmicroarray analysis of gene expression in endothelial cells in response to 24-hshear stress. Physiol Genomics, 2001, 7(1):55-63.
[11] Lovett JK, Rothwell PM. Site of carotid plaque ulceration in relation todirection of blood flow: an angiographic and pathological study. Cerebrovasc Dis,2003, 16(4):369-75.
[12] Danzi S, Klein I. Thyroid hormone and the cardiovascular system. MinervaEndocrinol, 2004, 29(3):139-50.
[13] Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med,2001, 344(7):501-9.
[14] Napoli R, Biondi B, Guardasole V, Matarazzo M, Pardo F, Angelini V, Fazio S,SaccaL. Impact of hyperthyroidism and its correction on vascular reactivity in humans.Circulation, 2001, 104(25):3076-80.
[15] Choudhury RP, MacDermot J. Heart failure in thyrotoxicosis, an approach tomanagement. Br J Clin Pharmacol, 1998, 46(5):421-4.
[16] Klein I, Ojamaa K. Thyrotoxicosis and the heart. Endocrinol Metab Clin North Am,1998, 27(1):51-62.
[17] Kiss E, Jakab G, Kranias EG,Edes I. Thyroid hormone-induced alterations inphospholamban protein expression. Regulatory effects on sarcoplasmic reticulumCa2+ transport and myocardial relaxation. Circ Res, 1994, 75(2):245-51.
[18] Fazio S, Palmieri EA, Lombardi G,Biondi B. Effects of thyroid hormone on thecardiovascular system. Recent Prog Horm Res, 2004, 59:31-50.
[19] Weinbrenner C, Gerbert B,Strasser RH. [Thyroid hormone and the cardiovascularsystem]. Dtsch Med Wochenschr, 2005, 130(39):2215-9.
[20] Buckey JC Jr, Lane LD, Levine BD, Watenpaugh DE, Wright SJ, Moore WE, GaffneyFA,Blomqvist CG. Orthostatic intolerance after spaceflight. J Appl Physiol, 1996,81(1):7-18.
[21] Arbeille P, Pottier JM, Fomina G, Roncin A,Kotovskaya A. Assessment of theinflight cardiovascular adaptation & deconditioning. (14 day Antares spaceflight).J Gravit Physiol, 1994, 1(1):P25-6.
[22] Convertino VA, Doerr DF,Stein SL. Changes in size and compliance of the calfafter 30 days of simulated microgravity. J Appl Physiol, 1989, 66(3):1509-12.
[23] Convertino VA, Doerr DF, Eckberg DL, Fritsch JM,Vernikos-Danellis J. Head-downbed rest impairs vagal baroreflex responses and provokes orthostatic hypotension.J Appl Physiol, 1990, 68(4):1458-64.
[24] 余志斌, 张立藩. 模拟失重大鼠心肌收缩性能降低的过程及其可逆性. 中华航空医学杂志,1994, 5(3):138-142.
[25] 陈杰, 张立藩. 长期模拟失重大鼠心肌收缩性能的改变. 中华航空医学杂志, 1995,6(1):42-46.
[26] 余志斌, 张立藩. 模拟失重大鼠心肌收缩性能降低涉及细胞钙转运机制. 中国应用生理学杂志, 1995, 11(2):97-101.
[27] 余志斌, 张立藩. 模拟失重大鼠心肌肌浆网Ca2＋摄取功能的变化. 航天医学与医学工程,1995, 8(2):84-88.
[28] 马进, 张立藩. 长期尾部悬吊对大鼠左心室乳头肌等长收缩性能的影响. 航天医学与医学工程, 1996, 9(1):49-53.
[29] 余志斌, 张立藩. 中,长期尾部悬吊大鼠心肌功能与结构的变化. 航天医学与医学工程, 1997,10(2):140-144.
[30] 陈杰, 张立藩. 长期尾部悬吊大鼠冠脉血统量的变化. 中国应用生理学杂志, 1994,10(3):198-201.
[31] Papadopoulos A, Delp MD. Effects of hindlimb unweighting on the mechanical andstructure properties of the rat abdominal aorta. J Appl Physiol, 2003, 94(2):439-45.
[32] Kesl LD, Engen RL. Effects of NaHCO3 loading on acid-base balance, lactateconcentration, and performance in racing greyhounds. J Appl Physiol, 1998,85(3):1037-43.
[33] Looft-Wilson RC, Gisolfi CV. Rat small mesenteric artery function after hindlimbsuspension. J Appl Physiol, 2000, 88(4):1199-206.
[34] Delp MD. Myogenic and vasoconstrictor responsiveness of skeletal musclearterioles is diminished by hindlimb unloading. J Appl Physiol, 1999, 86(4):1178-84.
[35] 毛秦雯, 张立藩. 尾部悬吊大鼠不同部位动脉血管的分化性结构重塑变化. 航天医学与医学工程, 1999, 12(2):92-96.
[36] Sangha DS, Vaziri ND, Ding Y,Purdy RE. Vascular hyporesponsiveness in simulatedmicrogravity: role of nitric oxide-dependent mechanisms. J Appl Physiol, 2000,88(2):507-17.
[37] Fung YC, Liu SQ. Elementary mechanics of the endothelium of blood vessels. JBiomech Eng, 1993, 115(1):1-12.
[38] Schmid-Schoenbein GW, Fung YC,Zweifach BW. Vascular endothelium-leukocyteinteraction; sticking shear force in venules. Circ Res, 1975, 36(1):173-84.
[39] Mondy JS, Lindner V, Miyashiro JK, Berk BC, Dean RH,Geary RL. Platelet-derivedgrowth factor ligand and receptor expression in response to altered blood flow invivo. Circ Res, 1997, 81(3):320-7.
[40] Wong LC, Langille BL. Developmental remodeling of the internal elastic lamina ofrabbit arteries: effect of blood flow. Circ Res, 1996, 78(5):799-805.
[41] 韩启德, 文允镒著. 血管生物学.北京：北京医科大学中国协和医科大学联合出版社,1997:148-9.
[42] Muller JM, Chilian WM,Davis MJ. Integrin signaling transduces shear stress--dependent vasodilation of coronary arterioles. Circ Res, 1997, 80(3):320-6.
[43] 陈卫军, 应大君. 血流切应力对动脉内皮增殖影响的在体研究. 中国病理生理杂志, 2002,18(2):128-130.
[44] Cho A, Mitchell L, Koopmans D,Langille BL. Effects of changes in blood flow rateon cell death and cell proliferation in carotid arteries of immature rabbits.Circ Res, 1997, 81(3):328-37.
[45] Jalil JE, Janicki JS, Pick R,Weber KT. Coronary vascular remodeling andmyocardial fibrosis in the rat with renovascular hypertension. Response tocaptopril. Am J Hypertens, 1991, 4(1 Pt 1):51-5.
[46] 王桂清, 钱国正, 杨永举. 脑血管血液动力学指标检测参数的参考值. 中华流行病学杂志,2003, 24(2):98-101.
[47] Van Gieson EJ, Murfee WL, Skalak TC,Price RJ. Enhanced smooth muscle cellcoverage of microvessels exposed to increased hemodynamic stresses in vivo. CircRes, 2003, 92(8):929-36.
[48] Barbee KA, Mundel T, Lal R,Davies PF. Subcellular distribution of shear stress atthe surface of flow-aligned and nonaligned endothelial monolayers. Am J Physiol,1995, 268(4 Pt 2):H1765-72.
[49] Ueba H, Kawakami M,Yaginuma T. Shear stress as an inhibitor of vascular smoothmuscle cell proliferation. Role of transforming growth factor-beta 1 and tissuetypeplasminogen activator. Arterioscler Thromb Vasc Biol, 1997, 17(8):1512-6.
[50] Redmond EM, Cullen JP, Cahill PA, Sitzmann JV, Stefansson S, Lawrence DA,Okada SS.Endothelial cells inhibit flow-induced smooth muscle cell migration: role ofplasminogen activator inhibitor-1. Circulation, 2001, 103(4):597-603.
[51] Langille BL, O'Donnell F. Reductions in arterial diameter produced by chronicdecreases in blood flow are endothelium-dependent. Science, 1986, 231(4736):405-7.
[52] Koller A, Kaley G. Endothelial regulation of wall shear stress and blood flow inskeletal muscle microcirculation. Am J Physiol, 1991, 260(3 Pt 2):H862-8.
[53] Koller A, Sun D,Kaley G. Role of shear stress and endothelial prostaglandins inflow- and viscosity-induced dilation of arterioles in vitro. Circ Res, 1993,72(6):1276-84.
[54] Cooke JP, Rossitch E Jr, Andon NA, Loscalzo J,Dzau VJ. Flow activates anendothelial potassium channel to release an endogenous nitrovasodilator. J ClinInvest, 1991, 88(5):1663-71.
[55] Owlya R, Vollenweider L, Trueb L, Sartori C, Lepori M, Nicod P,Scherrer U.Cardiovascular and sympathetic effects of nitric oxide inhibition at rest andduring static exercise in humans. Circulation, 1997, 96(11):3897-903.
[56] Hutcheson IR, Griffith TM, Pitman MR, Towart R, Gregersen M, Refsum H,Karlsson JO.Iodinated radiographic contrast media inhibit shear stress- and agonist-evokedrelease of NO by the endothelium. Br J Pharmacol, 1999, 128(2):451-7.
[57] Hutcheson IR, Griffith TM. Release of endothelium-derived relaxing factor ismodulated both by frequency and amplitude of pulsatile flow. Am J Physiol, 1991,261(1 Pt 2):H257-62.
[58] Rubanyi GM, Romero JC,Vanhoutte PM. Flow-induced release of endothelium-derivedrelaxing factor. Am J Physiol, 1986, 250(6 Pt 2):H1145-9.
[59] Awolesi MA, Widmann MD, Sessa WC,Sumpio BE. Cyclic strain increases endothelialnitric oxide synthase activity. Surgery, 1994, 116(2):439-44; discussion 444-5.
[60] Inoue N, Ramasamy S, Fukai T, Nerem RM,Harrison DG. Shear stress modulatesexpression of Cu/Zn superoxide dismutase in human aortic endothelial cells. CircRes, 1996, 79(1):32-7.
[61] Qiu Y, Tarbell JM. Interaction between wall shear stress and circumferentialstrain affects endothelial cell biochemical production. J Vasc Res, 2000,37(3):147-57.
[62] Chiu JJ, Lee PL, Chen CN, Lee CI, Chang SF, Chen LJ, Lien SC, Ko YC, UsamiS,Chien S. Shear stress increases ICAM-1 and decreases VCAM-1 and E-selectinexpressions induced by tumor necrosis factor-[alpha] in endothelial cells.Arterioscler Thromb Vasc Biol, 2004, 24(1):73-9.
[63] Harrison DG. Physiological aspects of vascular endothelial cell interactions inhypertension and atherosclerosis. Acta Anaesthesiol Scand Suppl, 1993, 99:10-5.
[64] Shyy JY, Chien S. Role of integrins in endothelial mechanosensing of shear stress.Circ Res, 2002, 91(9):769-75.
[65] Frame MD, Sarelius IH. Flow-induced cytoskeletal changes in endothelial cellsgrowing on curved surfaces. Microcirculation, 2000, 7(6 Pt 1):419-27.
[66] Fisslthaler B, Boengler K, Fleming I, Schaper W, Busse R,Deindl E. Identificationof a cis-element regulating transcriptional activity in response to fluid shearstress in bovine aortic endothelial cells. Endothelium, 2003, 10(4-5):267-75.
[67] Walpola PL, Gotlieb AI, Cybulsky MI,Langille BL. Expression of ICAM-1 and VCAM-1and monocyte adherence in arteries exposed to altered shear stress. ArteriosclerThromb Vasc Biol, 1995, 15(1):2-10.
[68] Mohan S, Hamuro M, Koyoma K, Sorescu GP, Jo H,Natarajan M. High glucose inducedNF-kappaB DNA-binding activity in HAEC is maintained under low shear stress butinhibited under high shear stress: role of nitric oxide. Atherosclerosis, 2003,171(2):225-34.
[69] Hay DC, Beers C, Cameron V, Thomson L, Flitney FW,Hay RT. Activation of NF-kappaBnuclear transcription factor by flow in human endothelial cells. Biochim BiophysActa, 2003, 1642(1-2):33-44.
[70] Ohura N, Yamamoto K, Ichioka S, Sokabe T, Nakatsuka H, Baba A, Shibata M,Nakatsuka T, Harii K, Wada Y, Kohro T, Kodama T,Ando J. Global analysis of shearstress-responsive genes in vascular endothelial cells. J Atheroscler Thromb, 2003,10(5):304-13.
[71] Malek AM, Izumo S. Control of endothelial cell gene expression by flow. J Biomech,1995, 28(12):1515-28.
[72] Brent GA. The molecular basis of thyroid hormone action. N Engl J Med, 1994,331(13):847-53.
[73] Klein I, Ojamaa K. Thyroid hormone-targeting the heart. Endocrinology, 2001,142(1):11-2.
[74] White P, Dauncey MJ. Differential expression of thyroid hormone receptor isoformsis strikingly related to cardiac and skeletal muscle phenotype during postnataldevelopment. J Mol Endocrinol, 1999, 23(2):241-54.
[75] Kahaly GJ, Dienes HP, Beyer J,Hommel G. Iodide induces thyroid autoimmunity inpatients with endemic goitre: a randomised, double-blind, placebo-controlledtrial. Eur J Endocrinol, 1998, 139(3):290-7.
[76] Kahaly GJ, Forster GJ. Somatostatin receptor scintigraphy in thyroid eye disease.Thyroid, 1998, 8(6):549-52.
[77] Davis PJ, Davis FB. Nongenomic actions of thyroid hormone on the heart. Thyroid,2002, 12(6):459-66.
[78] Buroker NE, Young ME, Wei C, Serikawa K, Ge M, Ning XH,Portman MA. The dominantnegative thyroid hormone receptor beta-mutant {Delta}337T alters PPAR{alpha}signaling in heart. Am J Physiol Endocrinol Metab, 2007, 292(2):E453-60.
[79] Morkin E. Regulation of myosin heavy chain genes in the heart. Circulation, 1993,87(5):1451-60.
[80] Dillmann WH. Biochemical basis of thyroid hormone action in the heart. Am J Med,1990, 88(6):626-30.
[81] Mintz G, Pizzarello R,Klein I. Enhanced left ventricular diastolic function inhyperthyroidism: noninvasive assessment and response to treatment. J ClinEndocrinol Metab, 1991, 73(1):146-50.
[82] Nelson VL, Legro RS, Strauss JF 3rd,McAllister JM. Augmented androgen productionis a stable steroidogenic phenotype of propagated theca cells from polycysticovaries. Mol Endocrinol, 1999, 13(6):946-57.
[83] Forfar JC, Muir AL, Sawers SA,Toft AD. Abnormal left ventricular function inhyperthyroidism: evidence for a possible reversible cardiomyopathy. N Engl J Med,1982, 307(19):1165-70.
[84] Polikar R, Burger AG, Scherrer U,Nicod P. The thyroid and the heart. Circulation,1993, 87(5):1435-41.
[85] Olshansky B. Management of atrial fibrillation after coronary artery bypass graft.Am J Cardiol, 1996, 78(8A):27-34.
[86] Gilligan DM, Ellenbogen KA,Epstein AE. The management of atrial fibrillation. AmJ Med, 1996, 101(4):413-21.
[87] Kudenchuk PJ. Atrial fibrillation pearls and perils of management. West J Med,1996, 164(5):425-34.
[88] Krahn AD, Klein GJ, Kerr CR, Boone J, Sheldon R, Green M, Talajic M, WangX,Connolly S. How useful is thyroid function testing in patients with recentonsetatrial fibrillation? The Canadian Registry of Atrial FibrillationInvestigators. Arch Intern Med, 1996, 156(19):2221-4.
[89] Monzani F, Di Bello V, Caraccio N, Bertini A, Giorgi D, Giusti C,Ferrannini E.Effect of levothyroxine on cardiac function and structure in subclinicalhypothyroidism: a double blind, placebo-controlled study. J Clin Endocrinol Metab,2001, 86(3):1110-5.
[90] Moruzzi P. [The endothelium and the autonomic nervous system]. Cardiologia, 1998,43(11):1139-40.
[91] Osman F, Gammage MD,Franklyn JA. Hyperthyroidism and cardiovascular morbidity andmortality. Thyroid, 2002, 12(6):483-7.
[92] Biondi B, Palmieri EA, Fazio S, Cosco C, Nocera M, Sacca L, Filetti S, LombardiG,Perticone F. Endogenous subclinical hyperthyroidism affects quality of life andcardiac morphology and function in young and middle-aged patients. J ClinEndocrinol Metab, 2000, 85(12):4701-5.
[93] Marchant C, Brown L,Sernia C. Renin-angiotensin system in thyroid dysfunction inrats. J Cardiovasc Pharmacol, 1993, 22(3):449-55.
[94] Sernia C, Marchant C, Brown L,Hoey A. Cardiac angiotensin receptors inexperimental hyperthyroidism in dogs. Cardiovasc Res, 1993, 27(3):423-8.
[95] Basset A, Blanc J, Messas E, Hagege A,Elghozi JL. Renin-angiotensin systemcontribution to cardiac hypertrophy in experimental hyperthyroidism: anechocardiographic study. J Cardiovasc Pharmacol, 2001, 37(2):163-72.
[96] Hu LW, Benvenuti LA, Liberti EA, Carneiro-Ramos MS,Barreto-Chaves ML. Thyroxineinducedcardiac hypertrophy: influence of adrenergic nervous system versus reninangiotensinsystem on myocyte remodeling. Am J Physiol Regul Integr Comp Physiol,2003, 285(6):R1473-80.
[97] Chen K, Carey LC, Valego NK, Liu J,Rose JC. Thyroid hormone modulates renin andANG II receptor expression in fetal sheep. Am J Physiol Regul Integr Comp Physiol,2005, 289(4):R1006-14.
[98] Ruiz M, Montiel M, Jimenez E,Morell M. Effect of thyroid hormones onangiotensinogen production in the rat in vivo and in vitro. J Endocrinol, 1987,115(2):311-5.
[99] Udelsman R, Norton JA, Jelenich SE, Goldstein DS, Linehan WM, Loriaux DL,ChrousosGP. Responses of the hypothalamic-pituitary-adrenal and renin-angiotensin axesand the sympathetic system during controlled surgical and anesthetic stress. JClin Endocrinol Metab, 1987, 64(5):986-94.
[100] Fukuyama K, Ichiki T, Takeda K, Tokunou T, Iino N, Masuda S, Ishibashi M,Egashira K, Shimokawa H, Hirano K, Kanaide H,Takeshita A. Downregulation ofvascular angiotensin II type 1 receptor by thyroid hormone. Hypertension, 2003,41(3):598-603.
[101] Kobori H, Ichihara A, Miyashita Y, Hayashi M,Saruta T. Local renin-angiotensinsystem contributes to hyperthyroidism-induced cardiac hypertrophy. J Endocrinol,1999, 160(1):43-7.
[102] Ojamaa K, Klemperer JD,Klein I. Acute effects of thyroid hormone on vascularsmooth muscle. Thyroid, 1996, 6(5):505-12.
[103] Martin WH 3rd, Korte E, Tolley TK,Saffitz JE. Skeletal muscle beta-adrenoceptordistribution and responses to isoproterenol in hyperthyroidism. Am J Physiol,1992, 262(4 Pt 1):E504-10.
[104] Capo LA, Sillau AH. The effect of hyperthyroidism on capillarity and oxidativecapacity in rat soleus and gastrocnemius muscles. J Physiol, 1983, 342:1-14.
[105] Celsing F, Blomstrand E, Melichna J, Terrados N, Clausen N, Lins PE,Jansson E.Effect of hyperthyroidism on fibre-type composition, fibre area, glycogen contentand enzyme activity in human skeletal muscle. Clin Physiol, 1986, 6(2):171-81.
[106] Sussman MA. When the thyroid speaks, the heart listens. Circ Res, 2001,89(7):557-9.
[107] Fox AW, Juberg EN, May JM, Johnson RD, Abel PW,Minneman KP. Thyroid status andadrenergic receptor subtypes in the rat: comparison of receptor density andresponsiveness. J Pharmacol Exp Ther, 1985, 235(3):715-23.
[108] Gunasekera RD, Kuriyama H. The influence of thyroid states upon responses of therat aorta to catecholamines. Br J Pharmacol, 1990, 99(3):541-7.
[109] Scivoletto R, Fortes ZB,Garcia-Leme J. Thyroid hormones and vascular reactivity:role of the endothelial cell. Eur J Pharmacol, 1986, 129(3):271-8.
[110] McAllister RM, Grossenburg VD, Delp MD,Laughlin MH. Effects of hyperthyroidism onvascular contractile and relaxation responses. Am J Physiol, 1998, 274(5 Pt1):E946-53.
[111] Park KW, Dai HB, Ojamaa K, Lowenstein E, Klein I,Sellke FW. The direct vasomotoreffect of thyroid hormones on rat skeletal muscle resistance arteries. AnesthAnalg, 1997, 85(4):734-8.
[112] Novitzky D, Cooper DK, Barton CI, Greer A, Chaffin J, Grim J,Zuhdi N.Triiodothyronine as an inotropic agent after open heart surgery. J ThoracCardiovasc Surg, 1989, 98(5 Pt 2):972-7; discussion 977-8.
[113] Peng Y, He S, Zhang X, Liu G,Xie J. [Effects of hypoxia and qigong on urinemalondialdehyde, superoxide dismutase and circulating endothelial cell in humansduring simulated weightlessness]. Space Med Med Eng (Beijing), 1998, 11(2):136-8.
[114] Zhang LF, Chen JE, Ding ZP,Ma J. Cardiovascular deconditioning effects of longtermsimulated weightlessness in rats. Physiologist, 1993, 36(1 Suppl):S26-7.
[115] Zhang LF, Mao QW, Ma J,Yu ZB. Effects of simulated weightlessness on arterialvasculature (an experimental study on vascular deconditioning). J Gravit Physiol,1996, 3(2):5-8.
[116] Bungo MW, Goldwater DJ, Popp RL,Sandler H. Echocardiographic evaluation of spaceshuttle crewmembers. J Appl Physiol, 1987, 62(1):278-83.
[117] Nicogossian AE, Charles JB, Bungo MW, Leach-Huntoon CS,Nicgossian AE.Cardiovascular function in space flight. Acta Astronaut, 1991, 24:323-8.
[118] Purdy RE, Wilkerson MK, Hughson RL, Norsk P,Watenpaugh DE. The cardiovascularsystem in microgravity: symposium summary. Proc West Pharmacol Soc, 2003, 46:16-27.
[119] Xiao X, Mukkamala R, Sheynberg N, Grenon SM, Ehrman MD, Mullen TJ, Ramsdell CD,Williams GH,Cohen RJ. Effects of simulated microgravity on closed-loopcardiovascular regulation and orthostatic intolerance: analysis by means ofsystem identification. J Appl Physiol, 2004, 96(2):489-97.
[120] Pottier JM, Patat F, Arbeille P, Pourcelot L, Massabuau P, Guell A,Gharib C.Cardiovascular system and microgravity simulation and inflight results. ActaAstronaut, 1986, 13(1):47-51.
[121] Goldstein MA, Edwards RJ,Schroeter JP. Cardiac morphology after conditions ofmicrogravity during COSMOS 2044. J Appl Physiol, 1992, 73(2 Suppl):94S-100S.
[122] 毛秦雯, 张立藩. 模拟失重大鼠不同部位动脉动脉血管壁超微结构的变化. 航天医学与医学工程, 1999, 12(4):249-253.
[123] Zhang LN, Zhang LF,Ma J. Simulated microgravity enhances vasoconstrictorresponsiveness of rat basilar artery. J Appl Physiol, 2001, 90(6):2296-305.
[124] Purdy RE, Duckles SP, Krause DN, Rubera KM,Sara D. Effect of simulatedmicrogravity on vascular contractility. J Appl Physiol, 1998, 85(4):1307-15.
[125] Purdy RE, Kahwaji CI. Vascular adaptation to microgravity: extending thehypothesis. J Appl Physiol, 2002, 93(3):1181-2; author reply 1182.
[126] 马进, 杨天德. 模拟失重对大鼠后肢动脉血管床血管反应性的影响. 航天医学与医学工程,1999, 12(4):254-257.
[127] 马进, 张乐宁. 尾部悬吊大鼠不同动脉肾上腺素受体介导的血管反应性变化. 中华航空航天医学杂志, 1998, 9(4):201-204.
[128] 张乐宁, 马进. 14 天尾部悬吊大鼠肠系膜血管床反应性的变化.中华航空航天医学杂志, 1998,9(2):81-84.
[129] 马进, 张立藩. 短期模拟失重大鼠不同部位动脉血管反应性变化的比较. 中华航空航天医学杂志, 1997, 8(2):74-78.
[130] 马进, 任新, 张立藩, 马孝武, 程九华. 模拟失重对大鼠腹主动脉L-Arg-NO-cGMP 通路的影响. 中国应用生理学杂志, 2006, 22(3):269-273.
[131] Gibbons GH, Dzau VJ. The emerging concept of vascular remodeling. N Engl J Med,1994, 330(20):1431-8.
[132] 张立藩, 余志斌. 航天飞行后心血管失调的外周效应器机制假说. 生理科学进展, 2001,32(1):13-17.
[133] Zhang LF, Ma J, Mao QW,Yu ZB. Plasticity of arterial vasculature during simulatedweightlessness and its possible role in the genesis of postflight orthostaticintolerance. J Gravit Physiol, 1997, 4(2):P97-100.
[134] Ma J, Zhang LF, Yu ZB,Zhang LN. Time course and reversibility of arterialvasoreactivity changes in simulated microgravity rats. J Gravit Physiol, 1997,4(2):P45-6.
[135] Vargas F, Moreno JM, Rodriguez-Gomez I, Wangensteen R, Osuna A, Alvarez-GuerraM,Garcia-Estan J. Vascular and renal function in experimental thyroid disorders.Eur J Endocrinol, 2006, 154(2):197-212.
[136] 张子泰, 侯英萍, 邓敬兰, 暴军香, 汪静, 宋武战, 马进. 甲状腺机能亢进大鼠腹主动脉与股动脉血管反应性的变化. 心脏杂志, 2006, 18(5):516-519,527.
[137] 郝光荣著. 实验动物学. 上海：第二军医大学出版社, 1999:192.
[138] 马进, 任新玲, 程九华, 马孝武, 张立藩, 杨天德. 模拟失重大鼠去内皮股动脉血管反应性的变化. 中华航空航天医学杂志, 2003, (04).
[139] Katusic ZS, Shepherd JT. Endothelium-derived vasoactive factors: II. Endotheliumdependentcontraction. Hypertension, 1991, 18(5 Suppl):III86-92.
[140] Somlyo AP, Somlyo AV. Signal transduction and regulation in smooth muscle. Nature,1994, 372(6503):231-6.
[141] 陈杰, 马进. 一种模拟长期失重影响的大鼠尾部悬吊模型. 空间科学学报, 1993,13(2):159-162.
[142] Morey-Holton ER, Globus RK. Hindlimb unloading rodent model: technical aspects. JAppl Physiol, 2002, 92(4):1367-77.
[143] Lee RM. Preservation of in vivo morphology of blood vessels for morphometricstudies. Scanning Microsc, 1987, 1(3):1287-93.
[144] van Veen TA, van Rijen HV,Jongsma HJ. Physiology of cardiovascular gap junctions.Adv Cardiol, 2006, 42:18-40.
[145] Fagiolino P, Eiraldi R,Vazquez M. The influence of cardiovascular physiology ondose/pharmacokinetic and pharmacokinetic/pharmacodynamic relationships. ClinPharmacokinet, 2006, 45(5):433-48.
[2] Grigioni M, Daniele C, D'Avenio G,Barbaro V. On the monodimensional approach tothe estimation of the highest reynolds shear stress in a turbulent flow. JBiomech, 2000, 33(6):701-8.
[3] Moore JA, Steinman DA,Ethier CR. Computational blood flow modelling: errorsassociated with reconstructing finite element models from magnetic resonanceimages. J Biomech, 1998, 31(2):179-84.
[4] Couteau B, Payan Y,Lavallee S. The mesh-matching algorithm: an automatic 3D meshgenerator for finite element structures. J Biomech, 2000, 33(8):1005-9.
[5] Cebral JR, Lohner R, Choyke PL,Yim PJ. Merging of intersecting triangulations forfinite element modeling. J Biomech, 2001, 34(6):815-9.
[6] Etave F, Finet G, Boivin M, Boyer JC, Rioufol G,Thollet G. Mechanical propertiesof coronary stents determined by using finite element analysis. J Biomech, 2001,34(8):1065-75.
[7] Malek AM, Alper SL,Izumo S. Hemodynamic shear stress and its role inatherosclerosis. JAMA, 1999, 282(21):2035-42.
[8] Rieder MJ, Carmona R, Krieger JE, Pritchard KA Jr,Greene AS. Suppression ofangiotensin-converting enzyme expression and activity by shear stress. Circ Res,1997, 80(3):312-9.
[9] Liu Y, Chen BP, Lu M, Zhu Y, Stemerman MB, Chien S,Shyy JY. Shear stressactivation of SREBP1 in endothelial cells is mediated by integrins. ArteriosclerThromb Vasc Biol, 2002, 22(1):76-81.
[10] Chen BP, Li YS, Zhao Y, Chen KD, Li S, Lao J, Yuan S, Shyy JY,Chien S. DNAmicroarray analysis of gene expression in endothelial cells in response to 24-hshear stress. Physiol Genomics, 2001, 7(1):55-63.
[11] Lovett JK, Rothwell PM. Site of carotid plaque ulceration in relation todirection of blood flow: an angiographic and pathological study. Cerebrovasc Dis,2003, 16(4):369-75.
[12] Danzi S, Klein I. Thyroid hormone and the cardiovascular system. MinervaEndocrinol, 2004, 29(3):139-50.
[13] Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med,2001, 344(7):501-9.
[14] Napoli R, Biondi B, Guardasole V, Matarazzo M, Pardo F, Angelini V, Fazio S,SaccaL. Impact of hyperthyroidism and its correction on vascular reactivity in humans.Circulation, 2001, 104(25):3076-80.
[15] Choudhury RP, MacDermot J. Heart failure in thyrotoxicosis, an approach tomanagement. Br J Clin Pharmacol, 1998, 46(5):421-4.
[16] Klein I, Ojamaa K. Thyrotoxicosis and the heart. Endocrinol Metab Clin North Am,1998, 27(1):51-62.
[17] Kiss E, Jakab G, Kranias EG,Edes I. Thyroid hormone-induced alterations inphospholamban protein expression. Regulatory effects on sarcoplasmic reticulumCa2+ transport and myocardial relaxation. Circ Res, 1994, 75(2):245-51.
[18] Fazio S, Palmieri EA, Lombardi G,Biondi B. Effects of thyroid hormone on thecardiovascular system. Recent Prog Horm Res, 2004, 59:31-50.
[19] Weinbrenner C, Gerbert B,Strasser RH. [Thyroid hormone and the cardiovascularsystem]. Dtsch Med Wochenschr, 2005, 130(39):2215-9.
[20] Buckey JC Jr, Lane LD, Levine BD, Watenpaugh DE, Wright SJ, Moore WE, GaffneyFA,Blomqvist CG. Orthostatic intolerance after spaceflight. J Appl Physiol, 1996,81(1):7-18.
[21] Arbeille P, Pottier JM, Fomina G, Roncin A,Kotovskaya A. Assessment of theinflight cardiovascular adaptation & deconditioning. (14 day Antares spaceflight).J Gravit Physiol, 1994, 1(1):P25-6.
[22] Convertino VA, Doerr DF,Stein SL. Changes in size and compliance of the calfafter 30 days of simulated microgravity. J Appl Physiol, 1989, 66(3):1509-12.
[23] Convertino VA, Doerr DF, Eckberg DL, Fritsch JM,Vernikos-Danellis J. Head-downbed rest impairs vagal baroreflex responses and provokes orthostatic hypotension.J Appl Physiol, 1990, 68(4):1458-64.
[24] 余志斌, 张立藩. 模拟失重大鼠心肌收缩性能降低的过程及其可逆性. 中华航空医学杂志,1994, 5(3):138-142.
[25] 陈杰, 张立藩. 长期模拟失重大鼠心肌收缩性能的改变. 中华航空医学杂志, 1995,6(1):42-46.
[26] 余志斌, 张立藩. 模拟失重大鼠心肌收缩性能降低涉及细胞钙转运机制. 中国应用生理学杂志, 1995, 11(2):97-101.
[27] 余志斌, 张立藩. 模拟失重大鼠心肌肌浆网Ca2＋摄取功能的变化. 航天医学与医学工程,1995, 8(2):84-88.
[28] 马进, 张立藩. 长期尾部悬吊对大鼠左心室乳头肌等长收缩性能的影响. 航天医学与医学工程, 1996, 9(1):49-53.
[29] 余志斌, 张立藩. 中,长期尾部悬吊大鼠心肌功能与结构的变化. 航天医学与医学工程, 1997,10(2):140-144.
[30] 陈杰, 张立藩. 长期尾部悬吊大鼠冠脉血统量的变化. 中国应用生理学杂志, 1994,10(3):198-201.
[31] Papadopoulos A, Delp MD. Effects of hindlimb unweighting on the mechanical andstructure properties of the rat abdominal aorta. J Appl Physiol, 2003, 94(2):439-45.
[32] Kesl LD, Engen RL. Effects of NaHCO3 loading on acid-base balance, lactateconcentration, and performance in racing greyhounds. J Appl Physiol, 1998,85(3):1037-43.
[33] Looft-Wilson RC, Gisolfi CV. Rat small mesenteric artery function after hindlimbsuspension. J Appl Physiol, 2000, 88(4):1199-206.
[34] Delp MD. Myogenic and vasoconstrictor responsiveness of skeletal musclearterioles is diminished by hindlimb unloading. J Appl Physiol, 1999, 86(4):1178-84.
[35] 毛秦雯, 张立藩. 尾部悬吊大鼠不同部位动脉血管的分化性结构重塑变化. 航天医学与医学工程, 1999, 12(2):92-96.
[36] Sangha DS, Vaziri ND, Ding Y,Purdy RE. Vascular hyporesponsiveness in simulatedmicrogravity: role of nitric oxide-dependent mechanisms. J Appl Physiol, 2000,88(2):507-17.
[37] Fung YC, Liu SQ. Elementary mechanics of the endothelium of blood vessels. JBiomech Eng, 1993, 115(1):1-12.
[38] Schmid-Schoenbein GW, Fung YC,Zweifach BW. Vascular endothelium-leukocyteinteraction; sticking shear force in venules. Circ Res, 1975, 36(1):173-84.
[39] Mondy JS, Lindner V, Miyashiro JK, Berk BC, Dean RH,Geary RL. Platelet-derivedgrowth factor ligand and receptor expression in response to altered blood flow invivo. Circ Res, 1997, 81(3):320-7.
[40] Wong LC, Langille BL. Developmental remodeling of the internal elastic lamina ofrabbit arteries: effect of blood flow. Circ Res, 1996, 78(5):799-805.
[41] 韩启德, 文允镒著. 血管生物学.北京：北京医科大学中国协和医科大学联合出版社,1997:148-9.
[42] Muller JM, Chilian WM,Davis MJ. Integrin signaling transduces shear stress--dependent vasodilation of coronary arterioles. Circ Res, 1997, 80(3):320-6.
[43] 陈卫军, 应大君. 血流切应力对动脉内皮增殖影响的在体研究. 中国病理生理杂志, 2002,18(2):128-130.
[44] Cho A, Mitchell L, Koopmans D,Langille BL. Effects of changes in blood flow rateon cell death and cell proliferation in carotid arteries of immature rabbits.Circ Res, 1997, 81(3):328-37.
[45] Jalil JE, Janicki JS, Pick R,Weber KT. Coronary vascular remodeling andmyocardial fibrosis in the rat with renovascular hypertension. Response tocaptopril. Am J Hypertens, 1991, 4(1 Pt 1):51-5.
[46] 王桂清, 钱国正, 杨永举. 脑血管血液动力学指标检测参数的参考值. 中华流行病学杂志,2003, 24(2):98-101.
[47] Van Gieson EJ, Murfee WL, Skalak TC,Price RJ. Enhanced smooth muscle cellcoverage of microvessels exposed to increased hemodynamic stresses in vivo. CircRes, 2003, 92(8):929-36.
[48] Barbee KA, Mundel T, Lal R,Davies PF. Subcellular distribution of shear stress atthe surface of flow-aligned and nonaligned endothelial monolayers. Am J Physiol,1995, 268(4 Pt 2):H1765-72.
[49] Ueba H, Kawakami M,Yaginuma T. Shear stress as an inhibitor of vascular smoothmuscle cell proliferation. Role of transforming growth factor-beta 1 and tissuetypeplasminogen activator. Arterioscler Thromb Vasc Biol, 1997, 17(8):1512-6.
[50] Redmond EM, Cullen JP, Cahill PA, Sitzmann JV, Stefansson S, Lawrence DA,Okada SS.Endothelial cells inhibit flow-induced smooth muscle cell migration: role ofplasminogen activator inhibitor-1. Circulation, 2001, 103(4):597-603.
[51] Langille BL, O'Donnell F. Reductions in arterial diameter produced by chronicdecreases in blood flow are endothelium-dependent. Science, 1986, 231(4736):405-7.
[52] Koller A, Kaley G. Endothelial regulation of wall shear stress and blood flow inskeletal muscle microcirculation. Am J Physiol, 1991, 260(3 Pt 2):H862-8.
[53] Koller A, Sun D,Kaley G. Role of shear stress and endothelial prostaglandins inflow- and viscosity-induced dilation of arterioles in vitro. Circ Res, 1993,72(6):1276-84.
[54] Cooke JP, Rossitch E Jr, Andon NA, Loscalzo J,Dzau VJ. Flow activates anendothelial potassium channel to release an endogenous nitrovasodilator. J ClinInvest, 1991, 88(5):1663-71.
[55] Owlya R, Vollenweider L, Trueb L, Sartori C, Lepori M, Nicod P,Scherrer U.Cardiovascular and sympathetic effects of nitric oxide inhibition at rest andduring static exercise in humans. Circulation, 1997, 96(11):3897-903.
[56] Hutcheson IR, Griffith TM, Pitman MR, Towart R, Gregersen M, Refsum H,Karlsson JO.Iodinated radiographic contrast media inhibit shear stress- and agonist-evokedrelease of NO by the endothelium. Br J Pharmacol, 1999, 128(2):451-7.
[57] Hutcheson IR, Griffith TM. Release of endothelium-derived relaxing factor ismodulated both by frequency and amplitude of pulsatile flow. Am J Physiol, 1991,261(1 Pt 2):H257-62.
[58] Rubanyi GM, Romero JC,Vanhoutte PM. Flow-induced release of endothelium-derivedrelaxing factor. Am J Physiol, 1986, 250(6 Pt 2):H1145-9.
[59] Awolesi MA, Widmann MD, Sessa WC,Sumpio BE. Cyclic strain increases endothelialnitric oxide synthase activity. Surgery, 1994, 116(2):439-44; discussion 444-5.
[60] Inoue N, Ramasamy S, Fukai T, Nerem RM,Harrison DG. Shear stress modulatesexpression of Cu/Zn superoxide dismutase in human aortic endothelial cells. CircRes, 1996, 79(1):32-7.
[61] Qiu Y, Tarbell JM. Interaction between wall shear stress and circumferentialstrain affects endothelial cell biochemical production. J Vasc Res, 2000,37(3):147-57.
[62] Chiu JJ, Lee PL, Chen CN, Lee CI, Chang SF, Chen LJ, Lien SC, Ko YC, UsamiS,Chien S. Shear stress increases ICAM-1 and decreases VCAM-1 and E-selectinexpressions induced by tumor necrosis factor-[alpha] in endothelial cells.Arterioscler Thromb Vasc Biol, 2004, 24(1):73-9.
[63] Harrison DG. Physiological aspects of vascular endothelial cell interactions inhypertension and atherosclerosis. Acta Anaesthesiol Scand Suppl, 1993, 99:10-5.
[64] Shyy JY, Chien S. Role of integrins in endothelial mechanosensing of shear stress.Circ Res, 2002, 91(9):769-75.
[65] Frame MD, Sarelius IH. Flow-induced cytoskeletal changes in endothelial cellsgrowing on curved surfaces. Microcirculation, 2000, 7(6 Pt 1):419-27.
[66] Fisslthaler B, Boengler K, Fleming I, Schaper W, Busse R,Deindl E. Identificationof a cis-element regulating transcriptional activity in response to fluid shearstress in bovine aortic endothelial cells. Endothelium, 2003, 10(4-5):267-75.
[67] Walpola PL, Gotlieb AI, Cybulsky MI,Langille BL. Expression of ICAM-1 and VCAM-1and monocyte adherence in arteries exposed to altered shear stress. ArteriosclerThromb Vasc Biol, 1995, 15(1):2-10.
[68] Mohan S, Hamuro M, Koyoma K, Sorescu GP, Jo H,Natarajan M. High glucose inducedNF-kappaB DNA-binding activity in HAEC is maintained under low shear stress butinhibited under high shear stress: role of nitric oxide. Atherosclerosis, 2003,171(2):225-34.
[69] Hay DC, Beers C, Cameron V, Thomson L, Flitney FW,Hay RT. Activation of NF-kappaBnuclear transcription factor by flow in human endothelial cells. Biochim BiophysActa, 2003, 1642(1-2):33-44.
[70] Ohura N, Yamamoto K, Ichioka S, Sokabe T, Nakatsuka H, Baba A, Shibata M,Nakatsuka T, Harii K, Wada Y, Kohro T, Kodama T,Ando J. Global analysis of shearstress-responsive genes in vascular endothelial cells. J Atheroscler Thromb, 2003,10(5):304-13.
[71] Malek AM, Izumo S. Control of endothelial cell gene expression by flow. J Biomech,1995, 28(12):1515-28.
[72] Brent GA. The molecular basis of thyroid hormone action. N Engl J Med, 1994,331(13):847-53.
[73] Klein I, Ojamaa K. Thyroid hormone-targeting the heart. Endocrinology, 2001,142(1):11-2.
[74] White P, Dauncey MJ. Differential expression of thyroid hormone receptor isoformsis strikingly related to cardiac and skeletal muscle phenotype during postnataldevelopment. J Mol Endocrinol, 1999, 23(2):241-54.
[75] Kahaly GJ, Dienes HP, Beyer J,Hommel G. Iodide induces thyroid autoimmunity inpatients with endemic goitre: a randomised, double-blind, placebo-controlledtrial. Eur J Endocrinol, 1998, 139(3):290-7.
[76] Kahaly GJ, Forster GJ. Somatostatin receptor scintigraphy in thyroid eye disease.Thyroid, 1998, 8(6):549-52.
[77] Davis PJ, Davis FB. Nongenomic actions of thyroid hormone on the heart. Thyroid,2002, 12(6):459-66.
[78] Buroker NE, Young ME, Wei C, Serikawa K, Ge M, Ning XH,Portman MA. The dominantnegative thyroid hormone receptor beta-mutant {Delta}337T alters PPAR{alpha}signaling in heart. Am J Physiol Endocrinol Metab, 2007, 292(2):E453-60.
[79] Morkin E. Regulation of myosin heavy chain genes in the heart. Circulation, 1993,87(5):1451-60.
[80] Dillmann WH. Biochemical basis of thyroid hormone action in the heart. Am J Med,1990, 88(6):626-30.
[81] Mintz G, Pizzarello R,Klein I. Enhanced left ventricular diastolic function inhyperthyroidism: noninvasive assessment and response to treatment. J ClinEndocrinol Metab, 1991, 73(1):146-50.
[82] Nelson VL, Legro RS, Strauss JF 3rd,McAllister JM. Augmented androgen productionis a stable steroidogenic phenotype of propagated theca cells from polycysticovaries. Mol Endocrinol, 1999, 13(6):946-57.
[83] Forfar JC, Muir AL, Sawers SA,Toft AD. Abnormal left ventricular function inhyperthyroidism: evidence for a possible reversible cardiomyopathy. N Engl J Med,1982, 307(19):1165-70.
[84] Polikar R, Burger AG, Scherrer U,Nicod P. The thyroid and the heart. Circulation,1993, 87(5):1435-41.
[85] Olshansky B. Management of atrial fibrillation after coronary artery bypass graft.Am J Cardiol, 1996, 78(8A):27-34.
[86] Gilligan DM, Ellenbogen KA,Epstein AE. The management of atrial fibrillation. AmJ Med, 1996, 101(4):413-21.
[87] Kudenchuk PJ. Atrial fibrillation pearls and perils of management. West J Med,1996, 164(5):425-34.
[88] Krahn AD, Klein GJ, Kerr CR, Boone J, Sheldon R, Green M, Talajic M, WangX,Connolly S. How useful is thyroid function testing in patients with recentonsetatrial fibrillation? The Canadian Registry of Atrial FibrillationInvestigators. Arch Intern Med, 1996, 156(19):2221-4.
[89] Monzani F, Di Bello V, Caraccio N, Bertini A, Giorgi D, Giusti C,Ferrannini E.Effect of levothyroxine on cardiac function and structure in subclinicalhypothyroidism: a double blind, placebo-controlled study. J Clin Endocrinol Metab,2001, 86(3):1110-5.
[90] Moruzzi P. [The endothelium and the autonomic nervous system]. Cardiologia, 1998,43(11):1139-40.
[91] Osman F, Gammage MD,Franklyn JA. Hyperthyroidism and cardiovascular morbidity andmortality. Thyroid, 2002, 12(6):483-7.
[92] Biondi B, Palmieri EA, Fazio S, Cosco C, Nocera M, Sacca L, Filetti S, LombardiG,Perticone F. Endogenous subclinical hyperthyroidism affects quality of life andcardiac morphology and function in young and middle-aged patients. J ClinEndocrinol Metab, 2000, 85(12):4701-5.
[93] Marchant C, Brown L,Sernia C. Renin-angiotensin system in thyroid dysfunction inrats. J Cardiovasc Pharmacol, 1993, 22(3):449-55.
[94] Sernia C, Marchant C, Brown L,Hoey A. Cardiac angiotensin receptors inexperimental hyperthyroidism in dogs. Cardiovasc Res, 1993, 27(3):423-8.
[95] Basset A, Blanc J, Messas E, Hagege A,Elghozi JL. Renin-angiotensin systemcontribution to cardiac hypertrophy in experimental hyperthyroidism: anechocardiographic study. J Cardiovasc Pharmacol, 2001, 37(2):163-72.
[96] Hu LW, Benvenuti LA, Liberti EA, Carneiro-Ramos MS,Barreto-Chaves ML. Thyroxineinducedcardiac hypertrophy: influence of adrenergic nervous system versus reninangiotensinsystem on myocyte remodeling. Am J Physiol Regul Integr Comp Physiol,2003, 285(6):R1473-80.
[97] Chen K, Carey LC, Valego NK, Liu J,Rose JC. Thyroid hormone modulates renin andANG II receptor expression in fetal sheep. Am J Physiol Regul Integr Comp Physiol,2005, 289(4):R1006-14.
[98] Ruiz M, Montiel M, Jimenez E,Morell M. Effect of thyroid hormones onangiotensinogen production in the rat in vivo and in vitro. J Endocrinol, 1987,115(2):311-5.
[99] Udelsman R, Norton JA, Jelenich SE, Goldstein DS, Linehan WM, Loriaux DL,ChrousosGP. Responses of the hypothalamic-pituitary-adrenal and renin-angiotensin axesand the sympathetic system during controlled surgical and anesthetic stress. JClin Endocrinol Metab, 1987, 64(5):986-94.
[100] Fukuyama K, Ichiki T, Takeda K, Tokunou T, Iino N, Masuda S, Ishibashi M,Egashira K, Shimokawa H, Hirano K, Kanaide H,Takeshita A. Downregulation ofvascular angiotensin II type 1 receptor by thyroid hormone. Hypertension, 2003,41(3):598-603.
[101] Kobori H, Ichihara A, Miyashita Y, Hayashi M,Saruta T. Local renin-angiotensinsystem contributes to hyperthyroidism-induced cardiac hypertrophy. J Endocrinol,1999, 160(1):43-7.
[102] Ojamaa K, Klemperer JD,Klein I. Acute effects of thyroid hormone on vascularsmooth muscle. Thyroid, 1996, 6(5):505-12.
[103] Martin WH 3rd, Korte E, Tolley TK,Saffitz JE. Skeletal muscle beta-adrenoceptordistribution and responses to isoproterenol in hyperthyroidism. Am J Physiol,1992, 262(4 Pt 1):E504-10.
[104] Capo LA, Sillau AH. The effect of hyperthyroidism on capillarity and oxidativecapacity in rat soleus and gastrocnemius muscles. J Physiol, 1983, 342:1-14.
[105] Celsing F, Blomstrand E, Melichna J, Terrados N, Clausen N, Lins PE,Jansson E.Effect of hyperthyroidism on fibre-type composition, fibre area, glycogen contentand enzyme activity in human skeletal muscle. Clin Physiol, 1986, 6(2):171-81.
[106] Sussman MA. When the thyroid speaks, the heart listens. Circ Res, 2001,89(7):557-9.
[107] Fox AW, Juberg EN, May JM, Johnson RD, Abel PW,Minneman KP. Thyroid status andadrenergic receptor subtypes in the rat: comparison of receptor density andresponsiveness. J Pharmacol Exp Ther, 1985, 235(3):715-23.
[108] Gunasekera RD, Kuriyama H. The influence of thyroid states upon responses of therat aorta to catecholamines. Br J Pharmacol, 1990, 99(3):541-7.
[109] Scivoletto R, Fortes ZB,Garcia-Leme J. Thyroid hormones and vascular reactivity:role of the endothelial cell. Eur J Pharmacol, 1986, 129(3):271-8.
[110] McAllister RM, Grossenburg VD, Delp MD,Laughlin MH. Effects of hyperthyroidism onvascular contractile and relaxation responses. Am J Physiol, 1998, 274(5 Pt1):E946-53.
[111] Park KW, Dai HB, Ojamaa K, Lowenstein E, Klein I,Sellke FW. The direct vasomotoreffect of thyroid hormones on rat skeletal muscle resistance arteries. AnesthAnalg, 1997, 85(4):734-8.
[112] Novitzky D, Cooper DK, Barton CI, Greer A, Chaffin J, Grim J,Zuhdi N.Triiodothyronine as an inotropic agent after open heart surgery. J ThoracCardiovasc Surg, 1989, 98(5 Pt 2):972-7; discussion 977-8.
[113] Peng Y, He S, Zhang X, Liu G,Xie J. [Effects of hypoxia and qigong on urinemalondialdehyde, superoxide dismutase and circulating endothelial cell in humansduring simulated weightlessness]. Space Med Med Eng (Beijing), 1998, 11(2):136-8.
[114] Zhang LF, Chen JE, Ding ZP,Ma J. Cardiovascular deconditioning effects of longtermsimulated weightlessness in rats. Physiologist, 1993, 36(1 Suppl):S26-7.
[115] Zhang LF, Mao QW, Ma J,Yu ZB. Effects of simulated weightlessness on arterialvasculature (an experimental study on vascular deconditioning). J Gravit Physiol,1996, 3(2):5-8.
[116] Bungo MW, Goldwater DJ, Popp RL,Sandler H. Echocardiographic evaluation of spaceshuttle crewmembers. J Appl Physiol, 1987, 62(1):278-83.
[117] Nicogossian AE, Charles JB, Bungo MW, Leach-Huntoon CS,Nicgossian AE.Cardiovascular function in space flight. Acta Astronaut, 1991, 24:323-8.
[118] Purdy RE, Wilkerson MK, Hughson RL, Norsk P,Watenpaugh DE. The cardiovascularsystem in microgravity: symposium summary. Proc West Pharmacol Soc, 2003, 46:16-27.
[119] Xiao X, Mukkamala R, Sheynberg N, Grenon SM, Ehrman MD, Mullen TJ, Ramsdell CD,Williams GH,Cohen RJ. Effects of simulated microgravity on closed-loopcardiovascular regulation and orthostatic intolerance: analysis by means ofsystem identification. J Appl Physiol, 2004, 96(2):489-97.
[120] Pottier JM, Patat F, Arbeille P, Pourcelot L, Massabuau P, Guell A,Gharib C.Cardiovascular system and microgravity simulation and inflight results. ActaAstronaut, 1986, 13(1):47-51.
[121] Goldstein MA, Edwards RJ,Schroeter JP. Cardiac morphology after conditions ofmicrogravity during COSMOS 2044. J Appl Physiol, 1992, 73(2 Suppl):94S-100S.
[122] 毛秦雯, 张立藩. 模拟失重大鼠不同部位动脉动脉血管壁超微结构的变化. 航天医学与医学工程, 1999, 12(4):249-253.
[123] Zhang LN, Zhang LF,Ma J. Simulated microgravity enhances vasoconstrictorresponsiveness of rat basilar artery. J Appl Physiol, 2001, 90(6):2296-305.
[124] Purdy RE, Duckles SP, Krause DN, Rubera KM,Sara D. Effect of simulatedmicrogravity on vascular contractility. J Appl Physiol, 1998, 85(4):1307-15.
[125] Purdy RE, Kahwaji CI. Vascular adaptation to microgravity: extending thehypothesis. J Appl Physiol, 2002, 93(3):1181-2; author reply 1182.
[126] 马进, 杨天德. 模拟失重对大鼠后肢动脉血管床血管反应性的影响. 航天医学与医学工程,1999, 12(4):254-257.
[127] 马进, 张乐宁. 尾部悬吊大鼠不同动脉肾上腺素受体介导的血管反应性变化. 中华航空航天医学杂志, 1998, 9(4):201-204.
[128] 张乐宁, 马进. 14 天尾部悬吊大鼠肠系膜血管床反应性的变化.中华航空航天医学杂志, 1998,9(2):81-84.
[129] 马进, 张立藩. 短期模拟失重大鼠不同部位动脉血管反应性变化的比较. 中华航空航天医学杂志, 1997, 8(2):74-78.
[130] 马进, 任新, 张立藩, 马孝武, 程九华. 模拟失重对大鼠腹主动脉L-Arg-NO-cGMP 通路的影响. 中国应用生理学杂志, 2006, 22(3):269-273.
[131] Gibbons GH, Dzau VJ. The emerging concept of vascular remodeling. N Engl J Med,1994, 330(20):1431-8.
[132] 张立藩, 余志斌. 航天飞行后心血管失调的外周效应器机制假说. 生理科学进展, 2001,32(1):13-17.
[133] Zhang LF, Ma J, Mao QW,Yu ZB. Plasticity of arterial vasculature during simulatedweightlessness and its possible role in the genesis of postflight orthostaticintolerance. J Gravit Physiol, 1997, 4(2):P97-100.
[134] Ma J, Zhang LF, Yu ZB,Zhang LN. Time course and reversibility of arterialvasoreactivity changes in simulated microgravity rats. J Gravit Physiol, 1997,4(2):P45-6.
[135] Vargas F, Moreno JM, Rodriguez-Gomez I, Wangensteen R, Osuna A, Alvarez-GuerraM,Garcia-Estan J. Vascular and renal function in experimental thyroid disorders.Eur J Endocrinol, 2006, 154(2):197-212.
[136] 张子泰, 侯英萍, 邓敬兰, 暴军香, 汪静, 宋武战, 马进. 甲状腺机能亢进大鼠腹主动脉与股动脉血管反应性的变化. 心脏杂志, 2006, 18(5):516-519,527.
[137] 郝光荣著. 实验动物学. 上海：第二军医大学出版社, 1999:192.
[138] 马进, 任新玲, 程九华, 马孝武, 张立藩, 杨天德. 模拟失重大鼠去内皮股动脉血管反应性的变化. 中华航空航天医学杂志, 2003, (04).
[139] Katusic ZS, Shepherd JT. Endothelium-derived vasoactive factors: II. Endotheliumdependentcontraction. Hypertension, 1991, 18(5 Suppl):III86-92.
[140] Somlyo AP, Somlyo AV. Signal transduction and regulation in smooth muscle. Nature,1994, 372(6503):231-6.
[141] 陈杰, 马进. 一种模拟长期失重影响的大鼠尾部悬吊模型. 空间科学学报, 1993,13(2):159-162.
[142] Morey-Holton ER, Globus RK. Hindlimb unloading rodent model: technical aspects. JAppl Physiol, 2002, 92(4):1367-77.
[143] Lee RM. Preservation of in vivo morphology of blood vessels for morphometricstudies. Scanning Microsc, 1987, 1(3):1287-93.
[144] van Veen TA, van Rijen HV,Jongsma HJ. Physiology of cardiovascular gap junctions.Adv Cardiol, 2006, 42:18-40.
[145] Fagiolino P, Eiraldi R,Vazquez M. The influence of cardiovascular physiology ondose/pharmacokinetic and pharmacokinetic/pharmacodynamic relationships. ClinPharmacokinet, 2006, 45(5):433-48.