Liver hemodynamics during portal venous endotoxemia in swine.

The acute hemodynamic response of the liver to portal endotoxemia was measured in six isoflurane anesthetized pigs in which volume support was used to maintain normal cardiac output. After baseline monitoring, bacterial endotoxin (LPS) was infused over 1 hr into a mesenteric vein at a rate of 1 microgram.kg-1.hr-1, and monitoring was continued for 1 hr postinfusion. Peak vasoconstriction occurred during LPS infusion in both the hepatic artery (resistance increases 349% of baseline, P < 0.05) and the liver's portal circulation (resistance increases 159% of baseline, P < 0.05). Increased vascular resistance was also detected in lung (increases 433% of baseline) and intestine (increases 130% of baseline) at the midpoint of the LPS infusion. The non-splanchnic circulation, defined for our analysis as all of the peripheral circulation except the portal and hepatic arterial circulation, generally exhibited little change in vascular resistance during LPS infusion. LPS was incompletely cleared by the liver, but secondary clearance by the lung prevented large increases in the LPS concentration of arterial blood. During the first hour postinfusion, the systemic vascular resistance subsequently decreased to near normal in all vascular beds, with the exception of the liver's portal circulation. A sustained and secondary increase in vascular resistance of the liver's portal circulation and portal vein pressure occurred during the first hour after LPS infusion. We conclude that most of the vasoconstriction in the acute response to portal endotoxemia occurs in the liver and lung, organs directly exposed to elevated levels of endotoxins.