【摘要】 杂交犬１４只，采用门静脉插管法，门脉内反复注射聚乙烯醇（ＰＶＡ），３个月后制成肝纤维化门脉高压症动物模型，出现脾大、腹水、食管静脉曲张等表现，门静脉造影显示门一体侧枝循环大量形成，病理检查显示肝细胞变性、坏死，肝纤维化形成。实验前后，分别测定门静脉压为９４．５±９．１ｍｍＨ２Ｏ（０．９３±０．０９ｋｐａ）和３０５．８±５７．９ｍｍＨ２Ｏ（３．００±０．５７ｋｐａ）（Ｘ±ｓ，ｎ＝１０，提示门脉高压症形成后，门脉压力明显升高（Ｐ＜０．００１）。结果与肝硬化门脉高压症临床表现相一致。为进一步研究肝内型门脉高压症发病机制提供了极为理想的动物模型。更多还原

【Abstract】 Portal hypertensive models of hapetic fibrosis were produced by intraportal polyvinyl alcohol(PVA) injections using portal cannulation in 14 mongrel dogs in 3 months.Splenomegaly,ascites and esophageal varices were demonstrated in these models,Portal visualization showed that porto-systemic collateral pathways had developed massively. Pathological examination showed that liver cells were of degeneration or necrosis,and hepatic fibrosis formed. Before and after the experiment,portal pressure were messured to be 94. 5±9.lmmH,O (0. 93 ± 0. 09kpa) and 305. 8±57. 9mmH2O(3. 00 ±0. 57kpa) (X ±s, n =10), respectively. It indcates that portal pressure increased pbviously(P<0. 001)after portal hypertension formed. The resuslt is cosistent with the clinical menifestation of cirrhotic portal hypertention. The research provides anexcellent animal model for making further study of pathogenic mechanism of intrahapetic portal hypertension.更多还原