Effect of Pitressin on the Splanchnic Circulation in Man

The effects of 20 units of pitressin administered intravenously on the splanchnic circulation in four patients without liver disease, 10 patients with cirrhosis and a patent portal vein, 11 patients with cirrhosis and an end-to-side portacaval anastomosis and two patients with an extrahepatic portal vein obstruction and a normal liver structure, were observed. Estimated hepatic blood flow and wedged hepatic venous and intrasplenic pressures were measured in all groups, and the splanchnic, hepatic arteriolar, and hepatic postsinusoidal resistances were calculated. Pitressin reduced the portal pressure by an average of 39 per cent for 1 hour. Estimated hepatic blood flow was reduced by 40 per cent. Splanchnic resistance was increased by 87 per cent and hepatic arteriolar resistance by 77 per cent. Postsinusoidal resistance was not affected. The drop in portal pressure could be related to the increases in splanchnic resistance. There was no difference in the response to pitressin between patients with cirrhosis and patients with normal liver structure and function. It is suggested that the fundamental lesion causing portal hypertension in cirrhosis is an obstruction to the hepatic venous outflow and that mesenteric and hepatic arteriolar venous anastomoses are not operative in the genesis of portal hypertension in cirrhosis. This obstruction to hepatic venous outflow is not alterable pharmacologically and any attempts to lower portal pressure by medical means must be achieved by alterations in the splanchnic resistance. Pitressin appears to be the most potent splanchnic vasoconstrictor available.