Does local sympathetic atrophy contribute to splanchnic vasodilation in portal hypertension?

摘要

Patients with cirrhosis have a generalized circulatory dysfunction with abnormalities in the splanchnic as well as in the systemic circulation (1). Increased intrahepatic vascular resistance together with increased splanchnic blood flow leads to portal hypertension, which gives rise to a number of complications such as the formation of oesophageal varices, ascites, hepatic encephalopathy, the hepatorenal syndrome and others (2). In addition, patients with cirrhosis and portal hypertension exhibit abnormalities in their systemic circulation in terms of a hyperdynamic circulation. This includes an increased cardiac output and heart rate and reduced systemic arterial blood pressure and systemic vascular resistance (1-4). Although the changes in the splanchnic and systemic haemodynamics appear simultaneously, the link between the two abnormal haemodynamic systems is largely unknown and the mechanism(s) responsible for the development of the hyperdynamic circulation and the central hypovolaemia are yet to be resolved. There is now a general consensus that systemic (preferentially splanchnic) arterial vasodilatation is one of the patho-physiological hallmarks in cirrhosis. This may be due to (i) increased levels of circulating vasodilators or (ii) hyporesponsiveness of resistance vessels to vasoconstrictors or both. The list of vasodilators that have been implicated in the pathogenesis of the systemic haemodynamic changes is long (3, 5).