| 特集名 | 門脈圧亢進症 | |
|---|---|---|
| 題名 | 門脈圧亢進症の病態生理 | |
| 発刊年月 | 2000年 05月 | |
| 著者 | 堀 直樹 | 京都府立医科大学第三内科／済生会京都府病院内科 |
| 著者 | 岡上 武 | 京都府立医科大学第三内科 |
| 【 要旨 】 | 肝硬変における門脈圧亢進症は肝内血管抵抗上昇と門脈流入血流量増大の2因子で規定される．肝硬変の肝内血管床では，肝障害に伴い類洞内皮や星細胞で過剰に産生されるエンドセリン－1による類洞内皮小孔収縮と類洞内皮機能低下に伴うeNOS活性低下による類洞内皮弛緩低下が生じ類洞内圧は上昇する．門脈圧亢進が生じると，門脈体循環シャント形成を引き起こし，末梢動脈拡張を経てNa貯留および循環血漿量増大が生じ全身腹部血流のhyperdynamic stateとなり門脈流入血流量が増大する．その過程で末梢，腹部動脈血管は拡張し，その原因としてNO産生亢進，サイトカイン，プロスタサイクリン，体液，神経性拡張物質，EDHFの関与や，最近ではCOの関与も指摘されている． | |
| Theme | Portal Hypertension | |
|---|---|---|
| Title | Pathophysiology of Portal Hypertension | |
| Author | Naoki Hori | Third Department of Internal Medicine, Kyoto Prefectural University of Medicine / Department of Internal Medicine, Saiseikai Kyoto Hospital |
| Author | Takeshi Okanoue | Third Department of Internal Medicine, Kyoto Prefectural University of Medicine |
| [ Summary ] | Portal hypertension in cases of liver cirrhosis is induced by the interaction of elevated intrahepatic resistance, to the flow by the portocollateral vessels and an increase in portal venous inflow. The increased sinusoidal vascular tone, which partly contributes to increased intrahepatic resistance in liver cirrhosis, is induced by the increased contraction of sinusoidal endothelial pores. This is caused by the overproduction of endothelin-1 in sinusoidal endothelial and hepatic stellate cells and the increased tension in sinusoidal cells, due to an impaired release of nitric oxide (NO) accompanied with endothelial dysfunction in the course of liver injury. Elevated portal pressure, due to chronic liver injury, induces the formation of portocollateral vessels. Periarterial vasodilatation occurs because of increased vasodilatatory substances causing impared liver dysfunction and leaking into the peripheral vasculature through the portocollateral vessels. Periarterial vasodilatation results in a relative state of undersaturation in vascular beds and causes both Na retension and plasma volume expansion, through baro- and volume receptor stimulation. This condition leads to systemic and splanchnic hyperdynamic circulation and an increase in portal venous inflow in liver cirrhosis. In the course of the development of hyperdynamic circulatory states, the dilatation of peripheral and splanchnic arteries is induced by the following factors: these are NO, cytokines, prostacyclin, humoral or neurogenic vasodilatatory substances, an endothelially derived hyperporizing factor, and carbon monoxide. All these factors have recently been considered. |
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