The Portal and Hepatic Venous System in Shock

Abstract

Pressures in the portal vein, left hepatic vein and inferior vena cava were measured in 35 dogs before and after a severe hemorrhage and after re-infusion of the shed blood. In another 5 dogs changes in liver volume, occurring under these conditions were studied. In 20 of the dogs radiographic studies of the portal vein, hepatic vein and vena cava were made before and after hemorrhage and after re-infusion of the shed blood. The rise in portal venous pressure following re-infusion began to decline soon after completion of the re-infusion and usually reached control levels within one to one-and-a-half hours. It thus appeared unlikely that progressive hepatic outflow obstruction could account for progressive deterioration of the animals by causing pooling or damming of blood in the liver and splanchnic bed. An apparently reversed pressure gradient between the left hepatic vein and inferior vena cava was found during severe oligemia in 7 out of 22 animals. Radiologic narrowing of the portal vein and to a lesser extent, of the left hepatic vein and inferior vena cava was observed during oligemia, with return to grossly normal, and not increased, caliber following re-infusion. No evidence of a sphincteric mechanism could be demonstrated in the left hepatic vein. Only in the very terminal stages, shortly before death, was evidence of pooling noted in the portal system. Pooling was not confined to this vascular bed but occurred, also, in the hepatic veins and inferior vena cava. Possibly widespread loss of tone occurs in the venous system throughout the body so that large volumes of blood may be accommodated without rise in pressure in veins with loose perivenous support. This final and progressive venomotor paralysis could account for the decreased venous return to the heart and the progressive deterioration of the animal.