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The increased portal pressure in these cases is caused by an increased intrahepatic vascular resistance. This resistance is caused by a non-manipulable component, namely fibrosis, and by a drug-manipulable component, namely the development of contractile myofibroblasts by activation of stellate cells. These myofibroblasts cause an increased vascular resistance by a deficiency of nitric oxide (NO). On the other hand, there is a decreased extrahepatic systemic vascular resistance, caused by an excess of NO. As a result, there is an increased splanchnic* inflow: an attempt to maintain liver perfusion. This increased inflow then leads to the maintenance of flow in the collaterals. Clinically this phenomenon manifests itself by an increased cardiac output, a systemic underfilling and a low blood pressure with an increased pulse.

[*splanchnic circulation' describes the blood flow to the abdominal gastrointestinal organs including the stomach, liver, spleen, pancreas, small intestine, and large intestine. ]

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