Portal hemodynamics and humoral factors involved in a portal hypertensive rabbit model.

Hemodynamic changes and certain humoral factors possibly responsible for splanchnic hyperemia in portal hypertensive rabbits created by partial portal vein ligation were studied. Portal pressure was significantly elevated after portal vein ligation and reached a climax on the second day. Then, it decreased but still remained at a plateau in a portal hypertensive state in the following days. Portal blood flow, measured with an electromagnetic flowmeter, had no significant change immediately after portal vein ligation and on post ligation day-1, but it increased significantly from the second day. Portal venous resistance rose significantly from the basal state immediately after portal vein ligation, then, it decreased from the second day, but still remained at a high resistance level as compared with the normal (p < 0.05). The levels of prostaglandin E2 and prostacyclin in the portal vein increased immediately after portal vein ligation but decreased on the second day. However, prostacyclin rose again on the fifth day. It is apparent from this study that once portal pressure or portal resistance increases, there is a surge of prostaglandin E2 and prostacyclin in the portal blood. Due to the vasodilation effect of prostacyclin, prostaglandin E2 and other possible vasodilators, portosystemic shunts are gradually produced, and splanchnic hyperemia develops in the portal hypertension. The initial mechanism of portal hypertension in this model was due mainly to an increase in resistance. At a later stage, increased splanchnic blood flow combined with increased resistance played an important role in the maintenance of portal hypertension.