Clinical Gastroenterology Vol.15 No.5(2)

Theme Portal Hypertension
Title Pathophysiology of Portal Hypertension
Publish Date 2000/05
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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