Wu Z Y
Ren-Ji Hospital, Shanghai Second Medical University.
Zhonghua Wai Ke Za Zhi. 1990 Mar;28(3):147-50, 189.
In order to pinpoint the site causing increased intrahepatic vascular resistance, we observed the relationship between hepatic pathologic changes and free portal pressure (FPP) during the development of CCl4-induced liver cirrhosis of rat. The results suggested that the degeneration necrosis and regeneration of liver cells, and consequent stenosis, or obliteration of sinusoidal spaces caused by the swelling and disarrangement of the liver cell plates led to the occurrence of portal hypertension. The possibility of pre- or post-sinusoidal obstruction was excluded by the manifestation of the pathologic lesions. It is the authors' belief that the exact site of the increased intrahepatic vascular resistance was most likely at the level of hepatic sinusoids. Furthermore, there was certain positive correlation between plasma glucagon concentration and FPP, indicating that glucagon was also involved in the pathogenesis of portal hypertension.