Hepatic blood flow and oxygen consumption after burn and sepsis.
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).


CONCLUSIONS
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.
Tadros
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Shriners Burns Institute and The University of Texas Medical Branch, Galveston, USA. tadros@hlkd.azr.nl
Traber
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Herndon
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D000704:Analysis of Variance; D000818:Animals; D001158:Arteries / Q000502:physiology; D001794:Blood Pressure; D002056:Burns / Q000150:complications / Q000503:physiopathology*; D002302:Cardiac Output; D004195:Disease Models, Animal; D005260:Female; D006439:Hemodynamics; D006975:Hypertension, Portal / Q000209:etiology / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology; D008099:Liver / Q000378:metabolism*; D008102:Liver Circulation; D010101:Oxygen Consumption; D011168:Portal System / Q000502:physiology; D011897:Random Allocation; D012772:Shock, Septic / Q000209:etiology / Q000503:physiopathology*; D013552:Swine; D013556:Swine, Miniature; D014655:Vascular Resistance