日本小児外科学会雑誌
Online ISSN : 2187-4247
Print ISSN : 0288-609X
ISSN-L : 0288-609X
小児肝外門脈閉塞症の成因に関する臨床的ならびに実験的研究
本名 敏郎
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ジャーナル フリー

1983 年 19 巻 4 号 p. 649-666

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Portial recanalization of the thrombosed portal vein and the development of multiple small collateral venous channels adjacent to the portal vein are presumed to account for the cavernous transformation of the portal vein. The importance of sepsis in association with fever and dehydration in neonatal period is stressed. Nevertheless, there is a high proportion of cases with no obviousetiology. Clinical findings of 36 cases under 16 years of age were analyzed and the results were as following. 1) The extrahepatic portal venous pressure did not decrease with aging. 2) Intrahepatic portal vein was patent in most instances and the occlusive process was not progressive. 3) The degree of hepatopetal collaterals was not correlated with age, but increased with aging in individual cases. 4) The mean portal venous pressure of the group with highly developed hepatopetal collaterals wassignificantly low relative to the groups with slightly and moderately developed collaterals. 5) Histological findings of the liver wer grouped as following; (a)hepatic fibrosis, (b)chronic cholagitis, (c)chronic hepatitis, (d)congest ion, (e)normal liver tissure group. 6) Some of the chronic hepatic lesions above mentioned were presumed to have caused the portal occlusion in neonatal age. Experiments were designed to study the effect of gradual portal venous occlusion on the development of hepatopetal and hepatofugal collateral veins in the rat. Young adult Sprague-Dawley rats were randamized into two groups; (A) sham-operated in ten rats, (B) operated in 20, with placement of ameroid constrictor around the portal trunk. Nine weeks after the application of the constrictor, portal venous pressure was elevated to a level about twice of normal range. Five patterns of collateral veins developed in responce to the extrahepatic portal vein occlusion; (a) vein directly bridging across the occluding ameroid constrictor, (b) paraesophageal and submucosal vein, (c) veins to the left adrenal and renal vein, (d) retroperitoneal vein,(e) veins in ometoparietal adhesions. The lumen size of the submucosal esophageal veins in group (B) increased threefold compared to in groug (A). The occluded portal vein and the surrouding hepatoduodenal ligament in group (B) contained three types of the cavernous hamangiorna-like structure. This structure consisted of partial recanalization of the thrombosed portal vein and the development of multiple small venous collateral channels adjacent to the portal vein. This experimental production of the cavenous hamangioma-like structure suggests the cavernous transformation in the clinical extrahepatic portal hypertension is proved to be acquired in origin excluding rare cases of the portal venous atresia.

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© 1983 特定非営利活動法人 日本小児外科学会

この記事はクリエイティブ・コモンズ [表示 - 非営利 - 継承 4.0 国際]ライセンスの下に提供されています。
https://creativecommons.org/licenses/by-nc-sa/4.0/deed.ja
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