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利用主動(dòng)脈瓣反流連續(xù)多普勒頻譜評價(jià)左室松弛時(shí)間常數(shù)Tau的動(dòng)物實(shí)驗(yàn)研究

發(fā)布時(shí)間:2018-03-07 15:17

  本文選題:左室松弛時(shí)間常數(shù) 切入點(diǎn):連續(xù)多普勒頻譜 出處:《中國人民解放軍醫(yī)學(xué)院》2012年碩士論文 論文類型:學(xué)位論文


【摘要】:目的:探討采用主動(dòng)脈瓣反流連續(xù)多普勒頻譜評價(jià)左室松弛時(shí)間常數(shù)(Tau)的新方法。 方法:選擇18條健康成年比格犬,首先開胸暴露心臟,縫制心包吊床。左側(cè)頸總動(dòng)脈穿刺動(dòng)脈鞘管至升主動(dòng)脈;超聲引導(dǎo)下經(jīng)動(dòng)脈鞘制作犬主動(dòng)脈瓣反流模型;由心尖處插入Millar測壓導(dǎo)管至左心室;在超聲引導(dǎo)下,移動(dòng)左側(cè)動(dòng)脈鞘管前端至左冠狀動(dòng)脈竇內(nèi),然后反復(fù)間斷注射塑料微球注入左冠狀動(dòng)脈竇,以左室舒張末壓升高≥5mmHg為標(biāo)準(zhǔn),誘發(fā)急性缺血性左室功能障礙。觀察20分鐘血流動(dòng)力學(xué)狀態(tài)穩(wěn)定后,靜脈滴注多巴酚丁胺或艾司洛爾改變左心室功能。在不同血流動(dòng)力學(xué)狀態(tài)下,心臟超聲探頭采集主動(dòng)脈瓣反流連續(xù)多普勒頻譜及其原始音頻信號,多導(dǎo)生理儀同步記錄左室壓力-時(shí)間曲線及其dp/dt時(shí)間曲線、主動(dòng)脈壓力曲線及心電圖。 在dp/dt曲線上測量-dp/dtmax大小及其在所處時(shí)間的左室壓力P,根據(jù)公式Tau=-P/(dp/dt),計(jì)算Tau導(dǎo)管。通過MATLAB數(shù)學(xué)軟件對主動(dòng)脈瓣反流頻譜原始音頻數(shù)據(jù)后處理,使頻譜線刷新時(shí)間約為300us,形成新的多普勒頻譜。在后處理的主動(dòng)脈瓣反流頻譜曲線上選取1m/s、2m/s、3m/s速度點(diǎn)的時(shí)間值t1、t2、t3,帶入相應(yīng)Tau計(jì)算公式[Tau=(t2-tl)/ln((ADP-C-4)/(ADP-C-16) Tau=(t3-tl)/ln((ADP-C-4)/(ADP-C-36))],計(jì)算出超聲法Tau超聲,并與Tau導(dǎo)管進(jìn)行相關(guān)性分析、差異性檢驗(yàn)和一致性檢驗(yàn)。 結(jié)果:18只犬全部成功制作中度主動(dòng)脈瓣反流模型,其中12只犬造成無冠瓣穿孔,6只犬右冠瓣穿孔。然后,通過反復(fù)多次注射微球法構(gòu)建急性缺血左室舒張功能障礙模型,16條犬成功,2條犬室顫死亡。Tau導(dǎo)管與Tau超聲進(jìn)行相關(guān)性檢驗(yàn),P=0.0000.05,兩者具有相關(guān)性,相關(guān)系數(shù)r==0.86。Tau導(dǎo)管與Tau超聲兩者進(jìn)行成組設(shè)計(jì)兩樣本比較的t檢驗(yàn),以P0.05為差異有統(tǒng)計(jì)學(xué)意義,Tau導(dǎo)管(52.062±14.852)ms,Tau超聲(49.457±15.339)ms,P=0.06840.05兩者差異無統(tǒng)計(jì)學(xué)意義。T導(dǎo)管與T超聲差值進(jìn)行Bland-Altman(標(biāo)準(zhǔn)差-平均差值法)分析,具有較好的一致性。 結(jié)論:超聲引導(dǎo)下通過介入法,可造成主動(dòng)脈瓣反流模型,創(chuàng)傷小、可靠;應(yīng)用微球反復(fù)注射入左冠狀動(dòng)脈竇法,可形成左室舒張功能障礙動(dòng)物模型,安全、可靠;測量主動(dòng)脈瓣反流連續(xù)多普勒頻譜上升支速度為1m/s、2m/s、3m/s的時(shí)間t1、t2、t3,帶入相應(yīng)Tau公式即可計(jì)算出Tau,與導(dǎo)管法比較具有良好相關(guān)性。
[Abstract]:Aim: to explore a new method for evaluating left ventricular relaxation time constant (Tau) using aortic regurgitation continuous Doppler spectrum. Methods: 18 healthy adult Beagle dogs were selected. The heart was exposed with open chest, pericardial hammock was sewn, left common carotid artery was punctured to ascending aorta, aortic valve regurgitation model was made by transarterial sheath under ultrasonic guidance. Millar pressure catheter was inserted into the left ventricle from the apex of the heart. Under the guidance of ultrasound, the left artery sheath was moved to the left coronary sinus, and then the plastic microspheres were repeatedly injected into the left coronary sinus. Acute ischemic left ventricular dysfunction was induced by elevation of left ventricular end-diastolic pressure 鈮,

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