The effect of a portacaval shunt on estimated hepatic blood flow and oxygen uptake in cirrhosis.

Analysis of hepatic hemodynamic adjustments is made peculiarly difficult by the complexity of the splanchnic circulation. Blood flow through the liver appears to be controlled by the interactions between four sets of vascular resistances: (a) those imposed between the aorta and the portal vein including the splenic, gastric, mesenteric, and colic arterioles; (b) those between the aorta and the sinusoids, the hepatic arterioles; (c) those between the portal vein and the sinusoids, the portal venules; and (d) those between the sinusoids and the hepatic veins. During the development of cirrhotic disease of the liver a fifth set of resistances between the portal vein and the inferior vena cava, i.e., the collateral circulation, becomes important in determining blood flow. The portal venous pressure and the sinusoidal pressure are, likewise, resultants of the interaction of these resistances and arterial pressure. A change in any one resistance alone will induce various changes in the rate of blood flow through all the others and will affect the pressures in both the portal vein and sinusoids. In the absence of quantitative data regarding these factors, therefore, any discussion of the dynamics of splanchnic flows and pressures must be guarded. Nevertheless, it has seemed reasonable to believe that portal hypertension develops during cirrhotic disease (initially, at least) as a result of increased resistance to portal venous flow into the liver. Hence the reduction in hepatic blood flow (3)