發(fā)布時(shí)間：2020-12-01 17:04

　　背景和目的：重癥急性胰腺炎（severe acute pancreatitis, SAP）是一種發(fā)病急、進(jìn)展快、并發(fā)癥多、病死率高的臨床嚴(yán)重疾病。全身炎性反應(yīng)綜合征（systemicinflammatory response syndrome, SIRS）是SAP發(fā)展至多器官功能障礙綜合征（multiple organs dysfunction syndrome, MODS）的前期表現(xiàn)，是其高病死率的主要原因。過度的炎性反應(yīng)可導(dǎo)致機(jī)體免疫功能下降，器官感染、功能受損等，進(jìn)而導(dǎo)致并發(fā)癥發(fā)生率明顯升高[1,2]，進(jìn)一步加重SAP病情的發(fā)展，形成惡性循環(huán)。因此，阻斷SIRS向MODS的進(jìn)展是降低SAP高病死率的關(guān)鍵。多形核中性粒細(xì)胞（polymorphonuclear neutrophils, PMN），是炎癥反應(yīng)的重要效應(yīng)細(xì)胞，在炎癥的發(fā)生、發(fā)展和轉(zhuǎn)歸中起著關(guān)鍵的作用[3]。PMN凋亡障礙或延遲是SIRS的主要病理生理過程。鈣離子作為人體內(nèi)最普遍的信號(hào)轉(zhuǎn)導(dǎo)因子之一，調(diào)節(jié)著許多細(xì)胞和組織的生理活動(dòng)，其穩(wěn)態(tài)失衡是細(xì)胞凋亡的關(guān)鍵環(huán)節(jié)之一。本實(shí)驗(yàn)旨在SAP所致的SIRS大鼠模型中，研究PMN細(xì)胞內(nèi)... 

【文章來源】：大連醫(yī)科大學(xué)遼寧省

【文章頁(yè)數(shù)】：54 頁(yè)

【學(xué)位級(jí)別】：碩士

【部分圖文】：

正常大鼠與模型大鼠的大體解剖觀察

光鏡下胰腺組織病理學(xué)改變(HE染色20倍)

假手術(shù)組大鼠 SAP.SIRS 模型大鼠圖 1 正常大鼠與模型大鼠的大體解剖觀察假手術(shù)組 SAP.SIRS 模型組圖 2 光鏡下胰腺組織病理學(xué)改變(HE 染色 20 倍)

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