コリン欠乏性肝硬変における門脈圧亢進の発生原因

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タイトル別名
  • A decrease in vascular resistance in the sinusoid by elimination of fat deposition in the hepatic cell in the choline deficient diet induced cirrhosis of the rat liver.
  • コリン ケツボウセイ カンコウヘン ニ オケル モンミャクアツ コウシン ノ
  • 肝細胞内に蓄積した脂肪の除去による類洞血管抵抗の減少について

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Blood pressures along hepatic vascular path were measured in normal rats, and the choline deficient diet induced liver cirrhosis of rats with or without fat deposition in the hepatic cell. In the normal rat, the mean blood pressure was; 110mm H2O in the portal vein, 68mm H2O in the intrahepatic terminal portal vein, 28mm H2O in the central vein and 20mm H2O in the inferior vena cava. In the choline deficient diet induced cirrhosis of the liver, in which a marked fat deposition in the liver cell was seen and, as the result, the sinusoid was markedly narrowed, the blood pressures in the portal vein and the intrahepatic terminal portal vein significantly elevated to 173mm H2O and 100mm H2O, respectively, while no significant change in the blood pressure was recorded in the central vein and the inferior vena cava. In cirrhotic liver, in which fat deposition in the hepatic cell was eliminated by feeding the rat with the standard diet for two months and, as the result, the sinusoidal space was restored, the portal vein pressure was 137mm H2O and the intrahepatic terminal portal vein pressure was 72mm H2O, but there was no significant change in blood pressures in the central vein (32mm H2O) and the inferior vena cava (23mm H2O). Relationship between the hemodynamical data and the angiographical and histological changes of the liver was discussed. These results, particularly, a presence of a markedly increased vascular resistance in the intrahepatic portal vein as well as in the sinusoid and an unchanged vascular resistance in the hepatic vein in the choline deficient diet induced liver cirrhosis of rats, suggested that an increase in vascular resistance in the sinusoid and the intrahepatic portal vein were the important factors leading to portal hypertension, and that an increase in vascular resistance in the sinusoid was due to sinusoidal stenosis as the result of liver cell swelling which was curable.

収録刊行物

  • 肝臓

    肝臓 17 (2), 92-101, 1976

    一般社団法人 日本肝臓学会

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