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  本文選題：肝臟低灌注　切入點(diǎn)：缺血　出處：《第二軍醫(yī)大學(xué)學(xué)報(bào)》2016年05期

【摘要】：目的建立一種穩(wěn)定的小鼠肝臟持續(xù)低灌注模型,并在此基礎(chǔ)上研究肝臟持續(xù)低灌注對小鼠肝臟熱缺血再灌注損傷的影響。方法選用6~8周齡C57BL/6小鼠建模,將門靜脈縮窄至1mL注射器針頭直徑,門靜脈縮窄后3d、7d、14d和21d行肝功能及肝臟組織病理學(xué)檢測;選用穩(wěn)定的模型小鼠行70%缺血再灌注手術(shù),再灌注3h、24h、48h后行肝功能及肝臟組織病理學(xué)檢測。對照組采用正常C57BL/6小鼠行缺血再灌注手術(shù)。結(jié)果小鼠門靜脈縮窄術(shù)后,丙氨酸轉(zhuǎn)氨酶(ALT)和天冬氨酸轉(zhuǎn)氨酶(AST)均有不同程度的升高,在7d時達(dá)到高峰[ALT:(60.8±6.2)U/L vs(25.5±2.8)U/L,P0.001;AST:(74.9±6.1)U/L vs(39.1±3.2)U/L,P0.001),同時H-E染色顯示7d時肝細(xì)胞損傷最重,并且有較多炎細(xì)胞浸潤;在21d時,ALT基本恢復(fù)正常水平(P0.05),而AST仍高于正常水平(P=0.03)。低灌注處理7d的小鼠進(jìn)行缺血再灌注手術(shù)后,肝酶和組織病理學(xué)檢查顯示肝細(xì)胞損傷較對照組顯著加重,肝酶在再灌注3h達(dá)到高峰[ALT:(8 217.0±1 111.8)U/L vs(5 597.4±1 015.3)U/L,P=0.004;AST:(8 548.2±1 155.4)U/L vs(5 765.4±956.9)U/L,P=0.003];再灌注48h時,對照組小鼠ALT和AST均恢復(fù)正常,而經(jīng)過低灌注處理的小鼠肝酶仍高于對照組[ALT:(608.8±442.9)U/L vs(47.4±20.1)U/L,P=0.008;AST:(861.8±442.8)U/L vs(70.8±68.3)U/L,P=0.008)。結(jié)論成功建立了穩(wěn)定的小鼠肝臟持續(xù)低灌注模型,經(jīng)持續(xù)低灌注處理后的肝臟對熱缺血再灌注損傷的耐受能力顯著降低,這在一定程度上能夠模擬臨床上心死亡器官捐獻(xiàn)供肝的狀況。
[Abstract]:Objective to establish a stable model of liver continuous low perfusion in mice, and to study the effect of continuous low perfusion of liver on liver warm ischemia reperfusion injury in mice. Methods C57BL/6 mice at the age of 6 weeks and 8 weeks were used to model the model. The portal vein was constricted to the needle diameter of 1mL syringe, the liver function and hepatic histopathology were detected at 14 days and 21 days after portal vein coarctation, and 70% ischemia reperfusion operation was performed in stable model mice. Liver function and liver histopathology were detected after 3 h, 24 h and 48 h after reperfusion. Normal C57BL/6 mice were treated with ischemia reperfusion. Results after portal vein coarctation, alanine aminotransferase (alt) and aspartate aminotransferase (AST) increased in varying degrees. On the 7th day, the peak was reached [ALT:(60.8 鹵6.2)U/L vs(25.5 鹵2.8 U / L] P 0.001 + AST: 74.9 鹵6.1)U/L vs(39.1 鹵3.2U / L P 0.001.The H-E staining showed that the liver cells were most damaged and had more inflammatory cell infiltration on the 7th day. On the 21st day, alt returned to normal level basically, while AST was still higher than the normal level. Liver enzyme and histopathological examination showed that liver cell injury was significantly more serious than that of control group after ischemia reperfusion operation in mice treated with low perfusion for 7 days. The hepatic enzyme reached its peak at 3 h after reperfusion [ALT:(8 217.0 鹵1 111.8)U/L vs(5 597.4 鹵1 015.3U / L] [ALT:(8: 8 548.2 鹵1 155.4)U/L vs(5 765.4 鹵956.9 vs(5 765.4 鹵956.9U / L P0. 003], and the ALT and AST of the control group returned to normal at 48 h after reperfusion. However, the liver enzyme of mice treated with low perfusion was still higher than that of the control group [ALT:(608.8 鹵442.9)U/L vs(47.4 鹵20.1U / L ~ (-1) U / L] P _ (0.008) vs(70.8 ~ 861.8 鹵442.8)U/L vs(70.8 鹵68.3U / L ~ + P _ (0.008) .Conclusion A stable model of liver continuous low perfusion was established successfully, and the tolerance of liver treated with continuous low perfusion to hot ischemia / reperfusion injury was significantly decreased. To some extent, this can mimic the clinical status of donor liver donation of cardiac death organs.
【作者單位】： 第二軍醫(yī)大學(xué)長征醫(yī)院肝臟外科解放軍器官移植研究所;浙江大學(xué)醫(yī)學(xué)院附屬邵逸夫醫(yī)院頭頸外科;第二軍醫(yī)大學(xué)基礎(chǔ)部免疫學(xué)教研室;
【基金】：國家自然科學(xué)基金(81470900) 上海市自然科學(xué)基金(15ZR1414100)~~
【分類號】：R575;R-332

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