Hemodynamic changes after ligation of a major branch of the portal vein in rats: Comparison with rats with portal vein constriction

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Abstract

In chronic portal-hypertensive rat models, such as portal vein constriction or cirrhosis, the portal blood flow that effectively perfuses the hepatocytes is substantially reduced because of anatomical or functional shunts. It is possible therefore that a feedback mechanism from the liver to the splanchnic bed is responsible for the splanchnic hyperemia observed in chronic portal hypertension. To investigate the possible role of such a feedback mechanism, we examined the chronological changes in both portal and systemic hemodynamics in rats after ligation of a major branch of the portal vein that supplies about 80 of the liver circulation. Rats submitted to sham surgery and portal vein–constricted rats were also studied. Blood flow and portal-systemic shunting were measured by radioactive microsphere techniques. For 7 days after portalbranch ligation, transient portal hypertension resulted from an elevated portal resistance. However, no significant changes in portal venous inflow or splanchnic arteriolar resistance were found in the portal branch–ligated rats, whereas in the portal vein–constricted rats significant hyperdynamic changes in these parameters were noted. On the other hand, transient hyperdynamic changes occurred in the systemic circulation during the period from the fourth to the sixth day after portal-branch ligation, similar to those observed in the portal vein–constricted rats. The lack of hyperdynamic changes in the portal territory of the portal branch-ligated rats suggests that the splanchnic hyperemia found in chronic portal-hypertensive states is unlikely to be caused by a feedback mechanism from the ischemic hepatic parenchyma. The transient development of a systemic hyperdynamic circulation during the period when the perfused liver mass has not yet fully hypertrophied after portalbranch ligation suggests that such a hyperdynamic change may be related to the impairment of hepatic function. (Hepatology 1994;19:202–209).

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