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甲狀腺素對腸缺血—再灌注腸黏膜屏障功能的保護(hù)作用

發(fā)布時間:2018-06-15 07:12

  本文選題:甲狀腺素 + 缺血-再灌注; 參考:《延邊大學(xué)》2005年碩士論文


【摘要】:多器官功能障礙綜合征是目前臨床中嚴(yán)重創(chuàng)傷和感染常見的并發(fā)癥,其死亡率較高。目前研究認(rèn)識到腸道細(xì)菌移位是產(chǎn)生細(xì)胞因子、炎癥介子的一個重要因素,繼而導(dǎo)致多器官功能障礙綜合征與高代謝狀態(tài),而細(xì)菌移位是腸黏膜屏障功能受損的后果。腸黏膜受到破壞,腸道細(xì)菌移位,很快導(dǎo)致腸源性細(xì)菌感染,細(xì)菌內(nèi)毒素則會激活細(xì)胞因子的釋放,誘導(dǎo)瀑布效應(yīng)的產(chǎn)生,導(dǎo)致臟器損害,甚至危及患者的生命,故保護(hù)腸黏膜屏障功能具有重要的意義。甲狀腺素是機(jī)體重要的內(nèi)分泌激素之一,其不僅對于維持心、腦等臟器的功能具有重要意義,而且近年研究還發(fā)現(xiàn)其對于肺、肝等均具有較明顯的保護(hù)作用。本實驗?zāi)康脑谟谔接懩c缺血—再灌注24h時甲狀腺素的代謝異常和腸黏膜屏障破壞之間的關(guān)系,闡明補(bǔ)充外源性甲狀腺素對腸黏膜屏障功能保護(hù)的作用機(jī)制,為臨床防治多器官功能障礙綜合癥提供必要的理論基礎(chǔ)。方法:將Wistar大鼠39只隨機(jī)分為4組,即假手術(shù)組(S,n=12)、腸缺血—再灌注組(G,n=8)、腸缺血—再灌注+生理鹽水組(N,n=9)、腸缺血—再灌注+甲狀腺素組(T,n=10)。利用腸系膜上動脈央閉法制作大鼠腸缺血—再灌注模型,并補(bǔ)充外源性甲狀腺素。24h后測定外周血游離甲狀腺素、促甲狀腺素、磷酸肌酸激酶和門靜脈血內(nèi)毒素水平,同時做腸黏膜形態(tài)學(xué)檢查。結(jié)果:再灌注24h后,G組和N組的血清甲狀腺素水平明顯低于S組,兩者之間有
[Abstract]:Multiple organ dysfunction syndrome is a common complication of severe trauma and infection. At present, it has been recognized that intestinal bacterial translocation is an important factor in the production of cytokines and inflammatory mesons, which leads to multiple organ dysfunction syndrome and hypermetabolic state, and bacterial translocation is the consequence of impaired intestinal mucosal barrier function. Intestinal mucous membrane is destroyed, intestinal bacteria are translocated, intestinal bacterial infection is caused quickly, bacterial endotoxin activates the release of cytokines, induces waterfall effect, causes organ damage, and even endangers the life of patients. It is important to protect intestinal mucosal barrier function. Thyroxine is one of the most important endocrine hormones in the body. It not only plays an important role in maintaining the function of organs such as heart and brain, but also has obvious protective effects on lung and liver. The purpose of this study was to investigate the relationship between abnormal thyroid hormone metabolism and intestinal mucosal barrier damage at 24 h after intestinal ischemia-reperfusion, and to elucidate the mechanism of protective effect of exogenous thyroxine on intestinal mucosal barrier function. To provide the necessary theoretical basis for clinical prevention and treatment of multiple organ dysfunction syndrome. Methods: Thirty-nine Wistar rats were randomly divided into 4 groups: sham operation group (n = 12), intestinal ischemia / reperfusion group (n = 8), intestinal ischemia / reperfusion normal saline group (n = 9), intestinal ischemia / reperfusion thyroxine group (n = 10). The rat model of intestinal ischemia-reperfusion was established by the method of superior mesenteric artery closure. The levels of free thyroxine, thyrotropin, creatine phosphokinase and endotoxin in portal vein blood were determined 24 hours after supplementation of exogenous thyroxine. At the same time, the morphology of intestinal mucosa was examined. Results: the serum thyroxine levels in group G and group N were significantly lower than those in group S after 24 hours of reperfusion.
【學(xué)位授予單位】:延邊大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2005
【分類號】:R363

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