Shibayama Y, Nakata K
Hepatology. 1985 Jul-Aug;5(4):643-8. doi: 10.1002/hep.1840050421.
To determine the localization of increased vascular resistance in cirrhotic liver, blood pressures were measured by a direct cannulation method at several key points in the hepatic vascular pathway in normal and cirrhotic rats. Cirrhosis was produced by feeding a choline-deficient diet. Blood pressures in normal rats were 110 mm H2O in the portal vein, 68 mm H2O in the terminal portal venule, 28 mm H2O in the terminal hepatic venule and 20 mm H2O in the inferior vena cava. In cirrhotic rats, blood pressures in the portal vein and the terminal portal venule were 173 and 100 mm H2O, respectively, while those in the terminal hepatic venule and the inferior vena cava were elevated only slightly above normal. These hemodynamic data suggest that an increase in vascular resistance in cirrhotic liver is present in the intrahepatic portal vein and sinusoids, but not in intrahepatic hepatic vein. In cirrhotic liver, stenosis and distortion were found in peripheral branches of the portal vein, and sinusoidal stenoses and a decrease in sinusoidal space were recognized. Accordingly, it is suggested that the increase in vascular resistance in the intrahepatic portal vein and sinusoids correlate with these structural changes. Although severe stenoses and distortion were found in hepatic vein branches, it was thought that they do not contribute to portal hypertension because of lack of increase in vascular resistance in the intrahepatic hepatic vein.
为了确定肝硬化肝脏中血管阻力增加的部位,通过直接插管法测量了正常大鼠和肝硬化大鼠肝血管通路中几个关键点的血压。通过喂食胆碱缺乏饮食诱导肝硬化。正常大鼠门静脉血压为110 mm H2O,终末门静脉小静脉血压为68 mm H2O,终末肝小静脉血压为28 mm H2O,下腔静脉血压为20 mm H2O。在肝硬化大鼠中,门静脉和终末门静脉小静脉的血压分别为173和100 mm H2O,而终末肝小静脉和下腔静脉的血压仅略高于正常水平。这些血流动力学数据表明,肝硬化肝脏中血管阻力增加存在于肝内门静脉和肝血窦,而不是肝内肝静脉。在肝硬化肝脏中,门静脉外周分支出现狭窄和扭曲,肝血窦狭窄和肝血窦间隙减小。因此,提示肝内门静脉和肝血窦血管阻力增加与这些结构变化相关。虽然肝静脉分支发现严重狭窄和扭曲,但由于肝内肝静脉血管阻力未增加,认为它们与门静脉高压无关。