本文關(guān)鍵詞： 肺泡表面活性物質(zhì) 燒沖復合傷 肺泡Ⅱ型上皮細胞 肺損傷 大鼠　出處：《天津醫(yī)科大學》2015年碩士論文　論文類型：學位論文

【摘要】：目的:燒沖復合傷是兩種致傷因素(即燒傷和沖擊傷)同時或相繼疊加于機體而造成的一種復合損傷形式,其死亡率高,病情重,并發(fā)癥多,救治困難,一直以來是臨床亟待需要解決的問題。其中,急性肺損傷(ALI)/急性呼吸窘迫綜合征(ARDS)是燒沖復合傷早期死亡的主要原因之一。肺泡表面活性物質(zhì)(PS)是由肺泡II型上皮細胞分泌的一種脂蛋白,具有使肺泡表面張力降低,維持肺泡穩(wěn)定性,防止肺水腫,改善氧合的作用。本實驗通過建立模擬大鼠燒沖復合傷模型,結(jié)合應用外源性肺泡表面活性物質(zhì),探討其對重度燒沖復合傷肺損傷的作用,為臨床治療奠定基礎(chǔ)。方法:選取雄性SD大鼠300只,建立重度燒沖復合傷模型,用隨機數(shù)表法分為假傷組(S)、燒沖復合傷治療組(T)、燒沖復合傷對照組(C)。每組致傷前0h及傷后6h、24h、48h、72h共5個觀察時相點進行觀察,使用便攜式血氣分析儀行血氣分析檢測;應用大鼠肺功能儀器測定大鼠肺功能;免疫組織化學法檢測肺組織髓過氧化物酶的表達的變化;肺組織病理學觀察肺組織形態(tài)學變化;應用透射電鏡觀察肺的超微結(jié)構(gòu);用Western Blot法測定肺組織中肺表面活性物質(zhì)結(jié)合蛋白A含量的時相變化以及caspase3的時相變化。結(jié)果:1、血氣分析的變化:T組和C組大鼠傷后其氧分壓(PaO2)顯著下降,兩組之間比較,T組顯著高于C組(P0.05);T組和C組大鼠傷后其二氧化碳分壓(PaCO2)顯著升高,兩組之間比較,T組顯著低于C組(P0.05);T組乳酸含量在各時間點均明顯高于C組(P0.05)。2、肺功能的變化:傷后T組大鼠的深吸氣量、中心氣道阻力、肺順應性及組織彈性在24h時顯著優(yōu)于C組(P0.05),與S組無統(tǒng)計學差異(P0.05)。3、MPO的變化:T組與C組傷后各時間點均高于S組;C組大鼠肺組織MPO表達升高,浸潤程度較多。4、肺組織病理的變化:C組大鼠主要表現(xiàn)為局部肺泡腔破壞、消失,呈實性改變,纖維組織細胞增生,淋巴細胞、漿細胞、中性粒細胞浸潤,部分肺泡腔尚存,肺泡上皮細胞脫落,肺泡間隔腫脹、增寬、可見出血,漸進性加重的肺出血及肺水腫,支氣管上皮細胞腫脹,上述病變在傷后24h最為嚴重。T組大鼠大部分肺泡腔結(jié)構(gòu)尚存,淋巴細胞、漿細胞、中性粒細胞浸潤、水腫等病理改變程度明顯較C組輕。5、透射電鏡(TEM)顯示:S組大鼠肺組織超微結(jié)構(gòu)正常。T組與C組比較AECⅡ的超微結(jié)構(gòu)發(fā)生了系列顯著變化。6h T組可見有中性粒細胞浸潤,板層小體排空較C組少;24h T組較C組炎性細胞較少,板層小體密度有所增強,體積較均勻,環(huán)繞核仁排列;48h T組可見肺泡腔結(jié)構(gòu),板層小體排空較明顯、融合,體積大小不等且不規(guī)則,與C組相比較輕,未見巨大板層小體,細胞膜結(jié)構(gòu)有“胞吐”/“胞吸”現(xiàn)象;72h T組板層小體數(shù)目略有增加,未見巨大板層小體,體積大小尚均勻,排空略少,重新呈指環(huán)狀繞核排列。6、肺泡上皮細胞的TUNEL檢測顯示,6h,T陽性率=0.156,C陽性率=0.410;24h,T陽性率=0.129,C陽性率=0.340;48h,T陽性率=0.105,C陽性率=0.307;72h,T陽性率=0.110,C陽性率=0.316。說明各個時間點T陽性率均小于C陽性率。7、Western Blot法顯示,T組和C組SP-A從傷后6h起表達明顯低于S組,兩組之間比較,T組表達顯著高于C組(P0.05)。結(jié)論:重度燒沖復合傷大鼠傷后早期即出現(xiàn)急性肺損傷,經(jīng)氣管給予肺泡表面活性物質(zhì)后,可顯著改善大鼠肺泡的通氣和換氣功能,提高機體氧供,緩解急性肺損傷對全身的損害。
[Abstract]:Objective: burn is two kinds of injury factors (i.e. burn and blast injury) a composite damage form simultaneously or successively superimposed on the body caused by its high mortality rate, severe illness, complications, treatment difficulties, has been a clinical problem urgently to be solved. In the acute lung injury (ALI) / acute respiratory distress syndrome (ARDS) is one of the main causes of early death of burn blast combined injury. Pulmonary surfactant (PS) is a lipoprotein secreted by alveolar type II epithelial cells, with the alveolar surface tension decreased, maintain alveolar stability, prevent lung edema, improve oxygenation function. The simulated rat burn model, application of exogenous pulmonary surfactant combination on severe burn injury of lungs, lay the foundation for clinical treatment. Methods: selected 300 male SD rats, weight set The degree of burn blast combined injury model with randomly divided into sham injury group (S), burn treatment group (T), burn control group (C). Each group before injury and 0h after injury 6h, 24h, 48h, 72h a total of 5 observed time points were observed the use of portable blood gas analyzer, detection and analysis of blood gas; pulmonary function instrument using rat pulmonary function test in rats; myeloperoxidase in lung tissue was detected by immunohistochemical method the expression changes; learn to observe the morphological changes of lung tissue pathology; ultrastructure of lung by transmission electron microscopy; Determination of binding protein A in lung tissue of pulmonary surfactant using Western Blot method and phase change of Caspase3 phase changes. Results: 1. The changes of blood gas analysis: T group and C group rats after injury, the oxygen partial pressure (PaO2) decreased significantly between the two groups, T group was significantly higher than that of C group (P0.05); T group and C group after the second oxidation injury in rats 紕沖垎鍘，

本文編號：1459386