Opposite effects of XXXX on hepatic blood flow and @entity26 consumption after burn and @entity295 .

@entity1707 @entity295 @entity5694 @entity5721 @entity101 @entity26 @entity4770 @entity99 @entity526
BACKGROUND: Burn and @entity295 are associated with @entity99 and @entity5721 . This study examines the hypothesis that postburn treatment with the vasodilator @entity4770 would be beneficial for hepatic perfusion and oxygenation. METHODS: Female @entity1707 (n = 18, 20-25 kg) underwent laparotomy, during which ultrasonic flow probes were placed on the portal vein and the common hepatic artery. Catheters were inserted in the superior mesenteric and left hepatic veins. After 5 days, all animals were anesthetized and 12 of them received 40% total body surface area third-degree burn; 100 microg/kg @entity526 lipopolysaccharide (LPS) was intravenously administered 18 hours postburn. Burned animals were randomized to receive a constant infusion of iloprost (20 ng/kg per minute) or an equivalent amount of carrier solution (normal saline). All animals were studied for 42 hours. RESULTS: Burn caused a 2.5-fold increase in hepatic arterial vascular resistance (HAVR) and a 39% decrease in @entity99 ( @entity99 ). Postburn administration of iloprost did not improve the hepatic arterial hemodynamics (1.8-fold increase in HAVR and 38% decrease in @entity99 ). Post-LPS, @entity99 was significantly reduced to 22% of baseline and HAVR was 15-fold increased (P < 0.05 vs. baseline, ANOVA). In contrast, iloprost-treated animals did not show hepatic arterial vasoconstriction, as both @entity99 and HAVR remained baseline values during the endotoxic phase (P < 0.05 vs. nontreated group, ANOVA). Postburn iloprost treatment yielded a significant improvement in post-LPS portal venous blood flow (PVBF, 79% of baseline vs. 45% of baseline in nontreated animals, P < 0.05, ANOVA). Portal venous pressure showed 16% and 56% increases after burn and endotoxin, respectively. @entity101 did not occur in iloprost-treated animals, as portal venous pressure remained within baseline range (P < 0.05 vs. nontreated group, ANOVA). Burn and @entity5694 resulted in a significant decrease of hepatic @entity26 delivery (hDO2, 63% and 12% of baseline, respectively) and hepatic @entity26 consumption (hVO2, 61% and 21% of baseline, respectively). Only during the postburn endotoxic phase, iloprost improved hDO2 and hVO2 (140% and 79%, respectively; P < 0.05 vs. nontreated group, ANOVA). CONCLUSIONS: Postburn @entity4770 treatment appears to have no beneficial effects on hepatic perfusion early postburn. However, during the late postburn endotoxic phase, @entity4770 seems to significantly improve hepatic total blood flow and oxygenation. In addition, @entity4770 treatment attenuated burn- and endotoxin-induced portal @entity101 .
