中华肝胆外科杂志
中華肝膽外科雜誌
중화간담외과잡지
CHINESE JOURNAL OF HEPATOBILIARY SURGERY
2008年
4期
265-268
,共4页
许浩%施宝民%杨镇%王秀艳%马宏岩%穆庆岭%吴泰璜
許浩%施寶民%楊鎮%王秀豔%馬宏巖%穆慶嶺%吳泰璜
허호%시보민%양진%왕수염%마굉암%목경령%오태황
肝硬化%门静脉高压%内皮细胞窗孔%肝窦%电镜
肝硬化%門靜脈高壓%內皮細胞窗孔%肝竇%電鏡
간경화%문정맥고압%내피세포창공%간두%전경
Liver cirrhosis%Portal hypertension%Fenestra%Endothelial cell%Electron microscope
目的 该研究以硫代乙酰胺复制门脉高压大鼠模型,对成模后的大鼠肝脏超微结构进行观察,探讨门脉高压大鼠肝脏超微结构的变化.方法 50只大鼠分为造模组(40只)和正常对照组(10只).造模组采取前5周使用0.03%的硫代乙酰胺,后5周使用0.04%硫代乙酰胺作为其饮用水,共诱导10周成模.对成模大鼠测定肠系膜上静脉压力,取硬化后肝脏标本,对收集后标本行HE染色,同时行电子显微镜观察肝脏超微结构变化.结果 模型组内皮细胞窗孔数量明显少于对照组,同时,门静脉压力明显高于对照组.结论 肝窦毛细血管化在硫代乙酰胺诱导的肝硬化门脉高压发生中起重要作用,肝窦内皮细胞窗孔减少并减小,内皮细胞下基底膜形成使肝细胞与外界物质交换减少,导致细胞缺氧、代谢产物聚集,肝细胞坏死,最终导致门脉高压的发生.
目的 該研究以硫代乙酰胺複製門脈高壓大鼠模型,對成模後的大鼠肝髒超微結構進行觀察,探討門脈高壓大鼠肝髒超微結構的變化.方法 50隻大鼠分為造模組(40隻)和正常對照組(10隻).造模組採取前5週使用0.03%的硫代乙酰胺,後5週使用0.04%硫代乙酰胺作為其飲用水,共誘導10週成模.對成模大鼠測定腸繫膜上靜脈壓力,取硬化後肝髒標本,對收集後標本行HE染色,同時行電子顯微鏡觀察肝髒超微結構變化.結果 模型組內皮細胞窗孔數量明顯少于對照組,同時,門靜脈壓力明顯高于對照組.結論 肝竇毛細血管化在硫代乙酰胺誘導的肝硬化門脈高壓髮生中起重要作用,肝竇內皮細胞窗孔減少併減小,內皮細胞下基底膜形成使肝細胞與外界物質交換減少,導緻細胞缺氧、代謝產物聚集,肝細胞壞死,最終導緻門脈高壓的髮生.
목적 해연구이류대을선알복제문맥고압대서모형,대성모후적대서간장초미결구진행관찰,탐토문맥고압대서간장초미결구적변화.방법 50지대서분위조모조(40지)화정상대조조(10지).조모조채취전5주사용0.03%적류대을선알,후5주사용0.04%류대을선알작위기음용수,공유도10주성모.대성모대서측정장계막상정맥압력,취경화후간장표본,대수집후표본행HE염색,동시행전자현미경관찰간장초미결구변화.결과 모형조내피세포창공수량명현소우대조조,동시,문정맥압력명현고우대조조.결론 간두모세혈관화재류대을선알유도적간경화문맥고압발생중기중요작용,간두내피세포창공감소병감소,내피세포하기저막형성사간세포여외계물질교환감소,도치세포결양、대사산물취집,간세포배사,최종도치문맥고압적발생.
Objective To observe the ultrastructural changes in liver after portal hypertension in rats.Methods A total of 50 rats were divided into the model groups(40)and control groups(10).The rats in the model group accepted 0.03% TAA administration.Five weeks later,the concentration of TAA was changed to 0.04% for induction for 10 weeks to establish the model of portal hypertension.The pressure of superior mesenteric vein was determined and cirrhotic liver samples obtained.The ultrastructuraI changes of were observed under electron microscope.Results The fenestra quantity of endothelial cells was significantly lower in the model group(P<0.01).The portal vein pressure was markedly higher in the control group(P<0.01).Conclusion Hepatic sinusoid capillarization plays an important role in occurrence of portal hypertension.The fenestra of endothelial cells in hepatic sinusoid reduces and the diameter of fenestra decreases.The formation of basement membrane impaires the substance exchange between blood and hepatic cells,which results in oxygen deficiency,metabolic product accumulation and cell necrosis.