兔心臟淋巴循環(huán)阻滯后Ⅰ、Ⅲ型膠原蛋白變化的實驗研究
發(fā)布時間:2018-04-12 07:47
本文選題:兔 + 心臟淋巴 ; 參考:《泰山醫(yī)學院》2005年碩士論文
【摘要】:目的早在上世紀60年代國外許多學者就對心臟淋巴的解剖生理及病理做了大量研究,1963年Miller等把狗的心臟淋巴阻滯后通過觀察提出心臟淋巴循環(huán)障礙是心內(nèi)膜纖維化的重要機制。近些年來有學者提出心臟淋巴循環(huán)障礙與冠脈、心肌間質(zhì)纖維化存在著一定聯(lián)系。有學者阻滯山羊心臟淋巴后對冠狀動脈結(jié)構(gòu)作了急性期和慢性期的觀察,發(fā)現(xiàn)阻滯淋巴10-14天,冠狀動脈和小動脈內(nèi)膜內(nèi)皮腫脹,排列紊亂,中膜水腫,淺層和外膜纖維結(jié)締組織增生。60-180天動脈內(nèi)膜中膜水腫明顯減輕,但外膜和心肌間質(zhì)仍有纖維結(jié)締組織增生。結(jié)締組織增生是因為組織中未能通過淋巴回流的高濃度的蛋白刺激纖維母細胞增生所致。本研究通過觀察兔心臟淋巴循環(huán)阻滯后血清中Ⅰ型前膠原羧基端肽(PICP)、Ⅲ型前膠原氨基端肽(PIIINP)和血管緊張素Ⅱ(AngⅡ)的變化規(guī)律,并用原位雜交的方法測定不同觀察時間點心肌間質(zhì)Ⅰ、Ⅲ型膠原蛋白mRNA的表達,探討心臟淋巴循環(huán)阻滯后心肌間質(zhì)纖維化的機制。 方法將34只健康成年新西蘭白兔隨機分為實驗組和對照組,每組各半。用3%戊巴比妥鈉(30mg/kg)靜脈麻醉后,行氣管插管,連接小動物呼吸機,進行輔助呼吸,心電監(jiān)護,沿胸骨正中切口,切開胸骨,打開心包暴露心臟,分別于左右心室靠近心尖部注射10%亞甲蘭0.5ml,可見心外膜下向心底回流的淋巴干,沿淋巴干走行的方向分別將主動脈與肺動脈間和主動脈后方與右肺上動脈間的淋巴結(jié)群灼燒,結(jié)扎其遠端淋巴管,逐層關(guān)閉胸腔。對照組除不結(jié)扎淋巴管、灼燒淋巴結(jié)外其余同實驗組。分別于術(shù)前、術(shù)后3、7、14、30、60d取靜脈血,應(yīng)用ELISA法測定血清中PICP、PIIINP和AngⅡ的濃度;用原位雜交的方法測定各個觀察點Ⅰ、Ⅲ型膠原蛋白mRNA的表達。 結(jié)果實驗組AngⅡ與PICP、PIIINP在結(jié)扎兔心臟淋巴循環(huán)后3和60天與結(jié)扎前差異無顯著性,與相應(yīng)對照組無顯著性差異(P0.05);結(jié)扎后7、14和30天明顯高于術(shù)前且明顯高于相應(yīng)對照組(P0.05);對照組術(shù)前與術(shù)后無顯著性差異(P0.05)。PICP、PIIINP與AngⅡ有高度相關(guān)性(P0.05)。實驗組原位雜交實驗結(jié)果表明Ⅱ、Ⅲ型膠原蛋白mRNA的表達與血清中PICP、PIIINP的變化一致。 結(jié)論兔心臟淋巴循環(huán)阻滯后,心肌間質(zhì)中Ⅰ、Ⅲ型膠原蛋白于第7d開始合成增加,持續(xù)至30d,60d恢復正常。Ⅰ、Ⅲ型膠原蛋白增加是心臟淋巴循環(huán)阻滯后心肌間質(zhì)纖維化的原因之一
[Abstract]:Objective as early as the 1960s, many foreign scholars have done a lot of research on the anatomy, physiology and pathology of cardiac lymph nodes. In 1963, Miller et al showed that the dysfunction of cardiac lymphatic circulation was an important mechanism of endocardial fibrosis after cardiac lymphoid block in dogs.In recent years, some scholars have suggested that cardiac lymphatic circulatory disorder is related to coronary artery and myocardial interstitial fibrosis.Some scholars observed the structure of coronary artery in acute and chronic phase after blocking cardiac lymph nodes in goats. It was found that the endothelium of coronary artery and arteriole intima was swollen, disordered, and middle membrane edema was observed after 10 ~ 14 days of lymphatic block.Superficial and adventitia fibrous connective tissue proliferation. 60-180 days of arterial intima media edema significantly reduced, but there is still fibrous connective tissue proliferation in adventitia and myocardial stroma.Connective tissue hyperplasia is caused by the high concentration of protein in the tissue that fails to flow through lymphatic reflux to stimulate fibroblast proliferation.In this study, we observed the changes of procollagen type I carboxyl terminal peptide (PICPN), type 鈪,
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