论文部分内容阅读
目的 建立稳定的肝硬变门脉高压症模型。方法 对大鼠在左肾静脉周围去血管化后皮下注射四氯化碳，然后观察肝脏组织形态学、门静脉系血管压力及分布、肝外门静脉系及侧支循环变化。结果 实验性肝硬变在形成过程中历经肝细胞变性坏死， 纤维组织增生及假小叶形成过程。实验第５ 周始， 门静脉压力显著高于对照组（ Ｐ＜ ０ ．０５） ；实验第１５ 周时，食管静脉管径显著大于对照组（ Ｐ＜ ０ ．０５） 。结论 大鼠左肾静脉周围去血管化后皮下注射四氯化碳所诱导的大鼠肝硬变门脉高压症模型简便、可靠，可广泛应用于门脉高压症的实验研究。
Objective To establish a stable cirrhotic portal hypertension model. Methods The rats were injected with carbon tetrachloride (CTC) after the blood was deenoviated around the left renal vein. Then the liver histomorphology, the pressure and distribution of portal vein blood vessels, the extrahepatic portal vein and collateral circulation were observed. Results Experimental cirrhosis in the process of formation of liver cell degeneration and necrosis, fibrosis and pseudolobule formation process. At the end of the fifth week, the portal pressure was significantly higher than that of the control group (P <0.05). At the fifteenth week of the experiment, the diameter of the esophageal vein was significantly larger than that of the control group (P <0.05). Conclusions Rat model of cirrhosis induced by subcutaneous injection of carbon tetrachloride after de-vascularization of the left renal vein in rats is simple and reliable and can be widely used in the experimental study of portal hypertension.