Effect of portosystemic shunting on PGI2 and glucagon levels in humans

This study determined if the proposed mediators of splanchnic blood flow, prostacyclin and glucagon, were elevated in patients with portal hypertension undergoing portal systemic shunts.

Chronic portal hypertension results in increased portal venous pressure and increased splanchnic blood flow. Animal studies have suggested prostacyclin or glucagon, potent vasodilators, as potential mediators of this increased flow. Correlative clinical studies have been difficult to perform due to the wide variation in degree of portal-systemic shunting and the frequent association of parenchymal liver disease in patients with cirrhosis.

The authors measured portal and systemic hemodynamics in PGI2 and glucagon levels in patients with portal hypertension due to cirrhosis (partial portal systemic shunt) and Budd-Chiari syndrome (complete portal systemic shunt) undergoing portal systemic shunts and in porto normotensive patients undergoing exploratory laparotomies.

PGI2 levels in portal hypertension were significantly increased over normal, and prostacyclin in Budd-Chiari patients were increased significantly over patients with cirrhosis. Both PGI2 and portal venous pressure decreased significantly after portal systemic shunting, and prostacyclin levels correlated directly with portal venous pressure (R = 0.37, p < 0.05).

This is the first evidence in humans supporting the hypothesis that PGI2 is elevated in portal hypertension and is related to both the degree of portal venous obstruction and portal pressure. PGI2 probably has a role in the abnormal splanchnic hemodynamics of human portal hypertension.