SINUSOIDAL STENOSIS AS THE CAUSE OF PORTAL HYPERTENSION IN CHOLINE DEFICIENT DIET INDUCED FATTY CIRRHOSIS OF THE RAT LIVER
SINUSOIDAL STENOSIS AS THE CAUSE OF PORTAL HYPERTENSION IN CHOLINE DEFICIENT DIET INDUCED FATTY CIRRHOSIS OF THE RAT LIVER
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肝窦狭窄是缺乏胆碱饮食诱发大鼠脂肪性肝硬化门静脉高压的原因
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发表时间：
1974
期刊：
影响因子：
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通讯作者：
K. Nakata
中科院分区：
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作者：
Kazuyoshi Wada;K. Fujimoto;Yukimura Fujikawa;Y. Shibayama;Hideaki Mitsui;K. Nakata
通过测量门静脉压力、离体灌注肝脏的血流动力学分析、肝内血管树的直径测量以及对喂食缺乏胆碱饮食的大鼠的肝脏进行组织学和组织计量学检查，评估肝脏的解剖学病变是否导致门静脉高压的发生。平均门静脉压力从正常水平132 mm H2O升高至脂肪肝中的175 mm H2O，脂肪肝伴纤维化中升高至179 mm H2O，肝硬化中升高至218 mm H2O。在Ht 33.5%、灌注压135 mm H2O的条件下，离体灌注大鼠肝脏的肝血流量较正常水平明显下降，脂肪肝组为3.0 ml/g/min~1.2 ml/g/min，纤维化脂肪肝组为0.4 ml/g/min，脂肪肝硬化组为0.7 ml/g/min。肝窦前后血管未见异常，但肝细胞增大，肝窦间隙明显缩小。门脉高压与肝窦间隙缩小之间存在密切相关性。结缔组织增殖与肝血管阻力的增加没有太大关系。本实验表明，肝窦间隙的缩小是与胆碱缺乏饮食诱发的脂肪肝以及脂肪性肝硬化（肝窦高压）中门静脉高压的发展相关的解剖学病变。
The anatomical lesion of the liver is evaluated as being responsible for development of portal hypertension through measurement of portal vein pressures, hemodynamical analysis of Isolated perfused livers, diameter measurement of intrahepatic vascular trees, and histological as well as his‐tometrical examinations of the liver in rats fed with choline deficient diet. The mean portal vein pressure was elevated from the normal level, 132 mm H2O to 175 mm H2O In fatty liver, to 179 mm H2O In fatty liver with fibrosis, and to 218 mm H,0 in fatty cirrhosis of liver. The hepatic blood flow of the isolated perfused rat liver definitely decreased from the normal level, 3.0 ml/g/min to 1.2 ml/g/min in fatty liver, 0.4 ml/g/min in fatty liver with fibrosis and 0.7 ml/g/min in fatty cirrhosis of liver under the condition of Ht 33.5% and perfusion pressure 135 mm H2O. There was no abnormality in the pre‐and post sinusoidal vessel, but the space of sinusoid was markedly diminished, reciprocally, to the enlargement of the hepatic cells. An intimate correlationship existed between portal hypertension and reduction of sinusoidal space. Connective tissue proliferation did not have much to do with the increase in hepatic vascular resistance. The present experiment suggested that reduction of sinusoidal space was the anatomical lesion related to development of portal hypertension in choline deficient diet induced fatty liver as well as fatty cirrhosis of the liver (sinusoidal hypertension).