【摘要】 为证实肝纤维化在肝硬化门脉高压形成中的作用,我们用半自动图象分析仪测定了大鼠CCl₄肝硬化的肝脏胶原含量,同时用检压计测定了同组动物的门脉压力,分析了两者的相关件。结果表明,正常大鼠肝内胶原面积为3206.30±864.62μm²,肝硬化大鼠为32390.16±11879.98μm²,差异极显著（P<0.001）。前者与参考面积的比值为1.58±0.43%,后者为15.97±5.86%。正常鼠肝脏胶原面积与门脉压力梯度没有相关性,肝硬化鼠血管周围面积（r=0.44,P<0.05）、肝小叶内胶原面积（r=0.79,P<0.01）及肝内胶原总面积（r=0.76,P<0.01）均与门脉压力梯度呈显著正相关。结果提示,在CCl₄肝硬化大鼠,肝纤维化是导致门脉高压的重要原因之一,支持门脉高压形成的后向血流学说。更多还原

【Abstract】 To ascertain the role of hepatie fibrosis in the formation of portal hyper-tension in cirrhosis, the content of liver collagen was measured by semiautomatic imageanalysis system. The results showed that hepatic collagen area in cirrhotic rat was muchhigher than the normal rat （32390.16±11879.98 vs. 3206.30±864.26μm², P<0 .001）.The surface-density of hepatic collagen was 1.58±0.43% in the normal, and 15.97±5.86% in the cirrhotics. In the cirrhotic rat, there was a positive correlation betweenportal pressure gradient and the surface density of portal tracts （r=0.44, P<0.05 ）, orcollagen of hepatic lobule （r=0.79, P<0.01） or the sum of both （r=0.76, P<0.01）.These results concluded that hepatic fibrosis is a main factor producing portal hyperten-sion in the rats with CCl₄-induced cirrhosis.更多还原