Studies on Hemodynamics in Portalhypertension

Observation on Intrahepatic Hemodynamic Changes in A cute Intrahepatic Portal Obstruction

Abstract

The auther studies on the intrahepatic hemodynamics in experimentally induced acute portal obstruction in dogs.
The Silica suspension was injected into the intrahepatic portal vein and the changes of portal venous pressure, wedged hepatic venous pressure, hepatic artery blood flow, portal blood flow and portographic findings were observed. Furthermore the influences of the hepatic artery ligation and application of various drugs such as Adrenalin, Pitressin, Buscopan, Pyrethia, Pacatal, or Procain which affect the portal circulation were also investigated.
The results are summerized as follow:
1) The wedged hepatic venous pressure elevated in pallalel with elevation of portal venous pressure.
In the group the hepatic artery being ligated the pressure gradient gradually increased with elevation of the portal venous pressure, whereas in the groups the drugs being administrated these pressures elevated pallalel.
2) The portal blood flow was markedly decreased converse to elevation of the portal venous pressure, while the hepatic artery blood flow was gradually increased. The flow rate of portal vein and hepatic artery was in the ratio 4.79: 1 before injection of silica, but after injection upon the degree of 350mm H₂O of portal venous pressure, there were in ratio 2: 1.
3) In the portographic observation there were tendency that the portal vein was opened within the sphere of hepatic vein catheter obstruction, while on the other part the portal vein was obstructed.
Accordingly it is suggested that portal venous and wedged hepatic venous pressure elevation in the acute intrahepatic portal obstruction have been resulted from the portal venous pressure elevation due to mechanical obstruction of the portal bed, and the reflection of the elevated portal venous pressure to the hepatic vein through the opening portal branches and furthermore the elevation of the sinusoidal pressure caused by compensatory augmentation of the hepatic artery blood flow against the decrease of portal blood flow.