有狹窄的雙分叉血管湍流數(shù)值模擬—與動(dòng)脈粥樣硬化的關(guān)系.pdf

1、摘要摘要?jiǎng)用}粥樣硬化(AS)日益成為影響人類(lèi)健康的主要原因之一。血流動(dòng)力學(xué)的因素被認(rèn)為是影響AS發(fā)生和發(fā)展的一個(gè)關(guān)鍵因素。近年大量的離體〔invitro)細(xì)胞實(shí)驗(yàn)研究證實(shí)了湍流(特別是湍流剪應(yīng)力TSS)對(duì)AS的形成和發(fā)展有重要影響。而分叉血管中由于其管徑和流向等參數(shù)的改變，AS發(fā)生會(huì)導(dǎo)致出現(xiàn)湍流的機(jī)會(huì)增大。為了研究動(dòng)脈粥樣硬化分叉血管內(nèi)流動(dòng)的湍流特性及其對(duì)AS的影響，本文采用數(shù)值方法，對(duì)非定常情況下有病變的對(duì)稱和非對(duì)稱分叉血管的流動(dòng)特征

2、、壁面剪應(yīng)力及湍流特性(特別是雷諾切應(yīng)力)進(jìn)行了分析研究，主要得到如下結(jié)果:(1)對(duì)有狹窄的對(duì)稱分叉血管的研究表明，當(dāng)血管中出現(xiàn)單側(cè)病變時(shí)，病變會(huì)影響其對(duì)應(yīng)壁面的流動(dòng)，可能會(huì)導(dǎo)致無(wú)病變側(cè)發(fā)生粥樣硬化，從而使斑塊最后呈對(duì)稱分布。另外，在狹窄前端、后緣都會(huì)有低壁面剪應(yīng)力區(qū)(狹窄前端的低壁面剪應(yīng)力區(qū)很小)，從而說(shuō)明動(dòng)脈粥樣硬化可能向病變的兩側(cè)蔓延隨病變程度增大:(a)壁面剪應(yīng)力在最大狹窄附近峰值增大，且在狹窄下游，低壁面剪應(yīng)力變化加劇，變化區(qū)

3、域也相對(duì)增大:ro)雷諾切應(yīng)力的峰值也增大，且峰值越向中心區(qū)域靠近。這說(shuō)明隨著病變的加重，動(dòng)脈粥樣硬化的進(jìn)程會(huì)加快。另外，隨分叉角的增大，病變會(huì)加快向其周?chē)臄U(kuò)散(壁面剪應(yīng)力峰值增大)。但分叉角為600時(shí)的低壁面剪應(yīng)力變化相對(duì)平緩。(2)對(duì)有狹窄的非對(duì)稱分叉血管的研究表明，狹窄下游、頸外動(dòng)脈、頸動(dòng)脈竇內(nèi)和頸動(dòng)脈收縮段內(nèi)壁面(除竇內(nèi)有對(duì)稱狹窄情況外)都有渦旋存在(竇內(nèi)渦旋區(qū)大)壁面剪應(yīng)力和雷諾切應(yīng)力在竇內(nèi)變化最復(fù)雜(竇內(nèi)有狹窄的情況更為復(fù)

4、雜)，特別是在竇內(nèi)有對(duì)稱狹窄時(shí)，在竇的內(nèi)壁面狹窄下游壁面剪應(yīng)力和雷諾切應(yīng)力有較大變化雷諾應(yīng)力在竇內(nèi)值變化最大，分叉處次之，頸外動(dòng)脈處最小，所有這些都說(shuō)明竇內(nèi)和分叉附近是斑塊發(fā)生、發(fā)展的高發(fā)區(qū)。另外，在流場(chǎng)中竇及頸外動(dòng)脈的入口的內(nèi)壁面附近、狹窄后緣及竇的末端存在湍動(dòng)能負(fù)產(chǎn)生率區(qū)域(是濃度聚集的地方)，也可能會(huì)引起和加速粥樣硬化的發(fā)生。(3)通過(guò)對(duì)對(duì)稱與非對(duì)稱分叉血管的數(shù)值模擬，可看到非對(duì)稱分叉對(duì)其上游流動(dòng)的影響:比如，狹窄前端，在頸總動(dòng)脈

5、中有單側(cè)狹窄的頸動(dòng)脈的剪應(yīng)力的降幅要比頸總動(dòng)脈中有對(duì)稱狹窄的大(對(duì)稱分叉時(shí)有對(duì)稱狹窄的降幅大)頸總動(dòng)摘要AbstractAtherosclerosis(AS)isoneofthemaindiseasesthatafectmankind.Amongmanyfactorshemodynamicfactoristhoughtoftheimportantonewhichdeterminesthegenerationanddevelopmento

6、fAS.Anumberofexperimentalresearchinvitrocellculturesystemshavedemonstratedthatturbulence(especiallyturbulentshearstresses(TSS))playsanimportantroleininitiationanddevelopmentofAS.Turbulencealwayshappensinbifurcationsofves

7、selsduetoconstrictionthechangeofdiameterofvesselandflowdirection.ToinvestigatetheefectsofturbulentfeaturesontheinitiationanddevelopmentofASinbifurcationsofvesselsweuseanumericalmethodtosimulatetheunsteadyturbulentflowsin

8、symmetricandasymmetricbifurcationofvesselswithstenosis(intheassum訓(xùn)onofplanartwodimensionalflows).Themainresults二asbelow:1.Inthecaseofsymmetricbifurcationofvesselswhenthereisaonesidedconstrictioninthevesselthepathological

9、changealterstheturbulentflowontheoppositewallwhichmayleadstoformationofASonnormalwall.Itisindicatedthatatlastbloodblotwillbesymmetricallydistributed.InadditionlowWSSareasaredevelopedbothbehindandbeforetheconstrictionwhic

10、hmeansASmayexpandonbothsidesofconstriction.ItisalsoshownthatthelargestWSSnearthelipoftheconstrictionandthechangeoflowWSSandtheregionwherethechangeoccursincreasingwiththeaggravatedpathologicalchangeswhichindicatesthemorea

11、ggravatingpathologicalchangesthequickerdevelopmentofatherosclerosis.TheefectofbifurcationangleontheformationofASisfinallyinvestigatedandtheresultsshowthePathologicalchangesmayaggravateneartheconstrictionwiththeincreaseof

12、bifurcationangles.Buttheturbulentfeaturesarequitediferentbetweenthebifurcationislargerthanandlessthan6002.Inthecaseofasymmetricbifurcationofvesselsthereexistvorticesinthedownstreamofconstrictionintheexternalcarotidartery

13、(ECA)incarotidsinusneartheconstrictionofinternalcarotidartery(ICA)(thelargesteddiesisfoundincarotidsinus).WSSandReynoldsshearstresschangecomplicatedlyincarotidsinusespeciallywhentherearesymmetricstenosisincarotidsinus.Th

14、echangeofReynoldsshearstressinCarotidsinusisthebiggestandnearthebifurcationthesecondlargestmeanwhilethechangeofECAisthesmallest.Theseshowthatcarotidsinusandvesselbifurcationaretheareasliableofformationanddevelopmentofpla