Hepatic blood flow and oxygen consumption after burn and sepsis

T. Tadros, D. L. Traber, David Herndon

Research output: Contribution to journalArticle

29 Citations (Scopus)

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 μg/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 ANOYA). 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). Conclusio: 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.

Original languageEnglish (US)
Pages (from-to)101-108
Number of pages8
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume49
Issue number1
StatePublished - 2000
Externally publishedYes

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Oxygen Consumption
Sepsis
Liver
Analysis of Variance
Endotoxemia
Portal Hypertension
Wounds and Injuries
Hot Temperature
Liver Circulation
Oxygen
Portal Pressure
Hepatic Veins
Multiple Organ Failure
Body Surface Area
Hepatic Artery
Portal Vein
Reperfusion Injury
Ultrasonics
Cardiac Output
Reperfusion

Keywords

  • Endotoxin
  • Hepatic ischemia
  • Hepatic oxygen consumption
  • Hepatic reperfusion injury
  • Portal hypertension
  • Sepsis
  • Thermal trauma

ASJC Scopus subject areas

  • Surgery

Cite this

Hepatic blood flow and oxygen consumption after burn and sepsis. / Tadros, T.; Traber, D. L.; Herndon, David.

In: Journal of Trauma - Injury, Infection and Critical Care, Vol. 49, No. 1, 2000, p. 101-108.

Research output: Contribution to journalArticle

Tadros, T. ; Traber, D. L. ; Herndon, David. / Hepatic blood flow and oxygen consumption after burn and sepsis. In: Journal of Trauma - Injury, Infection and Critical Care. 2000 ; Vol. 49, No. 1. pp. 101-108.
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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 μg/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 ANOYA). 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). Conclusio: 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.",
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AB - 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 μg/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 ANOYA). 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). Conclusio: 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.

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