本文選題：睡眠呼吸暫停低通氣綜合征 + 阻塞性�。� 參考：《臨床耳鼻咽喉頭頸外科雜志》2015年19期

【摘要】：目的:探討慢性間歇低氧(CIH)對大鼠肺損傷的機(jī)制和依達(dá)拉奉的干預(yù)作用及可能機(jī)制。方法:采用隨機(jī)數(shù)字表法將96只雄性Wistar大鼠隨機(jī)分為正常對照組(UC組)、間歇低氧組(CIH組)、依達(dá)拉奉治療組(NE組)、低氧生理鹽水組(NS組),各亞組持續(xù)時間分別為1、2、3、4周,每個亞組6只大鼠。實驗結(jié)束后分別觀察各亞組大鼠肺組織蘇木精-伊紅病理變化、血氣檢測血氧分壓(PO2),采用化學(xué)法檢測肺組織MDA含量和SOD活性,實時熒光定量PCR檢測AngⅡmRNA。結(jié)果:UC組未見明顯病理損害,而CIH組肺泡壁水腫增厚,肺泡融合,肺間質(zhì)及支氣管上皮內(nèi)也可見中性粒細(xì)胞浸潤,且隨時間延長,病理損傷逐漸加重;與NS組相比,NE組出現(xiàn)病理損傷的時間較晚且程度較輕;各組亞組內(nèi)PO2未見差異;與UC組同一時間點比較,CIH組PO2明顯降低,而NE組較NS組有所恢復(fù);與UC及NE組比較,CIH組及NS組MDA含量于各個時間點均逐漸增加(P0.05),SOD活性于各個時間點均逐漸減少(P0.05);AngⅡmRNA的表達(dá)于各個時間點增加,于4周達(dá)高峰;與CIH組比較,NE組各指標(biāo)的變化過程受到抑制(P0.05)。CIH組AngⅡmRNA與SOD呈負(fù)相關(guān)(r=-0.904,P0.01);AngⅡmRNA與MDA呈正相關(guān)(r=0.782,P0.01)。結(jié)論:慢性間歇低氧可通過氧化應(yīng)激和激活A(yù)ngⅡ?qū)е路谓M織損傷,依達(dá)拉奉可能通過清除氧自由基,從而抵抗間歇低氧所致肺損傷。
[Abstract]:Aim: to investigate the mechanism of chronic intermittent hypoxia (CIH) on lung injury in rats and the possible mechanism of Edaravone. Methods: 96 male Wistar rats were randomly divided into normal control group (UC group), intermittent hypoxia group (CIH group), Edaravone treatment group (NE group) and hypoxic saline group (NS group). There were 6 rats in each subgroup. After the experiment, the pathological changes of hematoxylin and eosin in lung tissue of rats in each subgroup were observed. Blood gas was used to detect the partial pressure of oxygen (PO2), the content of MDA and the activity of SOD in lung tissue were detected by chemical method, and the Ang 鈪，

本文編號：2108865