Hepatic blood flow and oxygen consumption after burn and sepsis

Abstract

Background: Alteration in the hepatic circulation after burn and in sepsis seems to be an essential component in the development of multiple organ failure.

Methods: Female pigs (n = 12, 20-25 kg) were instrumented with ultrasonic flow probes 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 six of them received 40% total body surface area third-degree burn. A total of 100 microg/kg Escherichia coli LPS was intravenously administered at 18 hours after burn. All animals were studied for 42 hours.

Results: Thermal injury resulted in a 48% decrease in hepatic arterial blood flow despite maintenance of normal cardiac output, resulting in a fall in hepatic oxygen delivery rate. Portal venous blood flow showed a 32% increase at 4 hours after burn. Post-LPS portal blood flow was significantly reduced for a period of 8 hours (51% of baseline (bl), p < 0.05 analysis of variance [ANOVA]). The hepatic arterial blood supply was also significantly reduced (12-67% of bl, p < 0.05 ANOVA) during the first 4 hours after LPS, indicating loss of the hepatic arterial response. The following 12 hours, a hepatic reperfusion phase was observed with an elevation of the hepatic arterial blood flow to 152% of bl (p < 0.05 ANOVA). Postburn endotoxemia resulted in a significant decrease of hepatic oxygen delivery (88%) and hepatic oxygen consumption (79%). Although the burn injury did not affect the portal venous pressure, postburn endotoxemia caused a significant portal hypertension during a period of 8 hours (225% of bl, p < 0.05 ANOVA).

Conclusion: Postburn sepsis amplifies the selective vasconstrictive impact of thermal injury on hepatic arterial blood flow, yielding a pronounced ischemia/ reperfusion injury, associated with a critical reduction of hepatic oxygen delivery and consumption. A postburn septic challenge induces portal hypertension, which may account for previously documented gut barrier dysfunction.