【摘要】：目的 重癥角結(jié)膜干燥癥是由多種原因引起眼表及淚膜異常的疾病,常引起病人眼部不適,視物模糊及淚液不穩(wěn)定等,嚴(yán)重者會導(dǎo)致眼角膜、結(jié)膜病變,甚至引起視力喪失,嚴(yán)重影響患者的生活質(zhì)量。目前,臨床上可以根據(jù)患者病情的嚴(yán)重程度采取一些治療措施,但淚液的分泌的減少嚴(yán)重影響其治療效果和進(jìn)一步的眼科治療。血管化自體頜下腺移植以移植頜下腺分泌的唾液代替淚液,是近來開展的一種治療角結(jié)膜干燥癥的新方法,臨床研究已證實(shí)移植成功的病例,患者眼干癥狀得到改善,取得了良好的效果。 血管化自體移植頜下腺難免要經(jīng)歷失神經(jīng)和缺血再灌注過程,兩者均可能對腺體的分泌功能產(chǎn)生影響。有研究證實(shí)神經(jīng)遞質(zhì)的分泌不足和自主神經(jīng)受體信號轉(zhuǎn)導(dǎo)通路下調(diào)是移植頜下腺分泌功能紊亂的重要機(jī)制。移植的腺體除失神經(jīng)支配外,還經(jīng)歷了缺血再灌注的過程。目前缺血再灌注后頜下腺的損傷—應(yīng)激反應(yīng)尚缺乏研究。所以本研究推測缺血再灌注損傷可能是移植腺體早期功能減退或喪失的重要原因。 為進(jìn)一步探究缺血再灌注對移植頜下腺分泌功能狀態(tài)的影響,本實(shí)驗(yàn)建立了大鼠頜下腺原位缺血再灌注模型,在保留大鼠頜下腺分泌神經(jīng)分支支配下,探討單純?nèi)毖俟嘧⒑蟠笫箢M下腺的損傷—應(yīng)激反應(yīng)及經(jīng)歷缺血再灌注后大鼠頜下腺分泌功能的變化。 材料與方法 在保留頜下腺神經(jīng)分支支配的情況下,建立了大鼠頜下腺原位缺血再灌注模型。頜下腺經(jīng)歷缺血90min后分別再灌注1h、12h、24h、72h,并以此作為觀察取樣的時(shí)間點(diǎn)。本研究于頜下腺導(dǎo)管斷端插管,采用Schirmer實(shí)驗(yàn)來觀察各時(shí)間點(diǎn)大鼠頜下腺分泌情況。為進(jìn)一步觀察大鼠頜下腺經(jīng)歷缺血再灌注后的損傷—應(yīng)激反應(yīng),本研究通過HE染色觀察頜下腺的組織形態(tài)變化；通過透射電鏡觀察腺體緊密連接超微結(jié)構(gòu)的變化；通過檢測組織內(nèi)活性氧觀察腺體的氧應(yīng)激；通過TUNEL法檢測腺體組織細(xì)胞的凋亡情況。 結(jié)果 大鼠頜下腺經(jīng)歷缺血再灌注后1h和12h,腺體分泌量顯著降低,至再灌注72h腺體的分泌量逐漸恢復(fù)正常。組織學(xué)觀察發(fā)現(xiàn),經(jīng)歷缺血再灌注后,腺體組織開始出現(xiàn)水腫及炎細(xì)胞浸潤,至再灌注12h最為嚴(yán)重,后逐漸恢復(fù)至正常。超微結(jié)構(gòu)進(jìn)一步觀察,緊密連接在再灌注1h和12h變得模糊,電子密度降低。腺體組織活性氧水平及細(xì)胞凋亡情況也表現(xiàn)出相同的趨勢,表現(xiàn)為在經(jīng)歷再灌注1h和12h后,腺體組織內(nèi)活性氧信號增多及細(xì)胞凋亡水平的顯著增高。 結(jié)論 本研究觀察缺血再灌注引起的大鼠頜下腺早期的損傷—應(yīng)激反應(yīng),與大鼠頜下腺經(jīng)歷缺血再灌注后早期分泌功能降低的情況相符。本研究證實(shí)缺血再灌注損傷后引起的損傷—應(yīng)激反應(yīng)是移植腺體早期分泌功能低下的重要原因之一。
[Abstract]:Objective severe keratoconjunctival xerosis is a disease with abnormal surface and lacrimal film caused by a variety of reasons, often causing eye discomfort, blurred vision and unstable tear, etc. Serious cases may lead to corneal and conjunctival lesions. It even causes loss of vision, which seriously affects the quality of life of the patients. At present, some therapeutic measures can be taken according to the severity of the patient's condition, but the decrease of lacrimal secretion seriously affects the therapeutic effect and further ophthalmological treatment. Vascularized submandibular gland transplantation is a new method to treat keratoconjunctival xerosis with saliva secreted from submandibular gland transplantation instead of lacrimal fluid. Clinical studies have confirmed the successful transplantation of the submandibular gland, and the dry eye symptoms of the patients have been improved. Good results have been achieved. Vascularized autotransplantation of submandibular gland will inevitably undergo denervation and ischemia-reperfusion, both of which may affect the secretory function of the gland. It has been proved that insufficient secretion of neurotransmitters and down-regulation of the signal transduction pathway of autonomic nerve receptors are the important mechanisms of the dysfunction of submandibular gland secretion. In addition to denervation, the transplanted glands undergo ischemia-reperfusion. At present, there is still little research on the injury-stress response of submandibular gland after ischemia-reperfusion. Therefore, this study speculated that ischemia-reperfusion injury may be an important cause of early dysfunction or loss of graft glands. In order to further investigate the effect of ischemia-reperfusion on the secretory function of submandibular gland transplantation, a rat model of submandibular gland ischemia-reperfusion in situ was established, which was controlled by preserving the secretory nerve branches of the submandibular gland in rats. To investigate the injury-stress response of submandibular gland in rats after simple ischemia-reperfusion and the changes of submandibular gland secretory function after ischemia-reperfusion. Materials and methods A rat model of in situ ischemia reperfusion of submandibular gland was established by preserving the nerve branches of the submandibular gland. The submandibular gland was reperfused for 1 h, 12 h, 24 h, 72 h after 90min ischemia, and as a time point to observe the sampling. In this study, the submandibular gland secretion was observed by Schirmer test at different time points. In order to observe the injury-stress response of submandibular gland after ischemia-reperfusion, the morphological changes of submandibular gland were observed by HE staining, the ultrastructural changes of tight junctions were observed by transmission electron microscopy (TEM), and the histological changes of submandibular gland were observed by transmission electron microscopy (TEM). Oxygen stress of glands was observed by detecting reactive oxygen species (Ros) and apoptosis of glandular cells was detected by TUNEL method. Results 1 h and 12 h after ischemia-reperfusion, the secretion of submandibular gland decreased significantly, and gradually returned to normal at 72 h after reperfusion. Histological observation showed that edema and inflammatory cell infiltration began to occur in glandular tissue after ischemia-reperfusion, and then returned to normal gradually after 12 hours of reperfusion. Ultrastructural observation showed that the tight junctions became blurred and electron density decreased at 1h and 12h after reperfusion. The levels of reactive oxygen species (Ros) and apoptosis also showed the same trend in glandular tissue. After 1 h and 12 h of reperfusion, the signal of reactive oxygen species (Ros) and the level of apoptosis in glandular tissue increased significantly. Conclusion the early injury-stress response of submandibular gland induced by ischemia-reperfusion is consistent with the decrease of early secretory function of submandibular gland after ischemia-reperfusion in rats. [WT5 "HZ] conclusion [WT5" BZ] [WT5 "BZ] This study confirmed that injury-stress response induced by ischemia-reperfusion injury is one of the important reasons for the early secretory dysfunction of transplanted glands.
【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R782

【共引文獻(xiàn)】

相關(guān)期刊論文 前10條

1 李秀娥;楊悅;劉筱菁;郭宏梅;李華;;自體頜下腺移植術(shù)后護(hù)理[J];北京大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2010年01期

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相關(guān)博士學(xué)位論文 前10條

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相關(guān)碩士學(xué)位論文 前10條

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6 何巧玲;六月青多糖抗肝纖維化作用及其分子機(jī)制的實(shí)驗(yàn)研究[D];廣西醫(yī)科大學(xué);2013年

7 趙西博;苯腎上腺素對放射損傷早期大鼠頜下腺的保護(hù)作用及其分子機(jī)制研究[D];大連醫(yī)科大學(xué);2012年

8 李沙;中樞神經(jīng)系統(tǒng)損傷與神經(jīng)免疫調(diào)節(jié)功能相關(guān)信號鏈研究[D];北京協(xié)和醫(yī)學(xué)院;2013年

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10 陸森;抑制Kupffer Cell對大鼠肝臟切除微循環(huán)障礙的影響[D];安徽醫(yī)科大學(xué);2013年

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本文編號：2471946