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During the last decades research into complications of portal hypertension have focused on the extrahepatic and systemic manifestations. Apart from splanchnic haemodynamic complications owing to increased portal pressure, such as development of oesophageal varices and ascites due to increased splanchnic hydrostatic pressure, it has become evident that patients with portal hypertension exhibit multi-organ failure leaving few organs unaffected. In 1955, Kowalski and Abelman described elevated stroke volume and cardiac output and low systemic vascular resistance in one third of patients with cirrhosis.1 Since that time, many authors have confirmed the presence of a hyperdynamic circulation affecting the course of the disease and the prognosis in portal hypertensive patients. A considerable number of experimental and human studies have sought to reveal a pathogenetic link between portal hypertension and these extrahepatic alterations. The “peripheral arterial vasodilatation theory” was launched 20 years ago and modifications of this hypothesis have prevailed until today.2 A splanchnic arteriolar vasodilatation owing to increased activity of, for example, nitric oxide, tumour necrosis factor-α (TNF-α), endocannabinoids and other vasodilators, and the succeeding neuro-humoral counter-regulatory mechanisms explain many of the haemodynamic changes in portal hypertension.3 Plasma volume expansion and effective central hypovolaemia activates vasoconstrictor systems and secondary sodium–water retention.2 The vasodilatation precedes renal sodium and water retention and plasma volume expansion which correlates with activated counter-regulatory vasoconstrictor systems such as the sympathetic nervous system, the renin–angiotensin–aldosterone system, the …
Competing interests: None declared.
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