PMID- 14685102
OWN - NLM
STAT- MEDLINE
DCOM- 20040122
LR  - 20181113
IS  - 0003-4932 (Print)
IS  - 1528-1140 (Electronic)
IS  - 0003-4932 (Linking)
VI  - 239
IP  - 1
DP  - 2004 Jan
TI  - Opposite effects of prostacyclin on hepatic blood flow and oxygen consumption 
      after burn and sepsis.
PG  - 67-74
AB  - BACKGROUND: Burn and sepsis are associated with hepatic ischemia and reperfusion 
      injury. This study examines the hypothesis that postburn treatment with the 
      vasodilator prostacyclin would be beneficial for hepatic perfusion and 
      oxygenation. METHODS: Female pigs (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 Escherichia 
      coli 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 hepatic 
      arterial blood flow (HABF). Postburn administration of iloprost did not improve 
      the hepatic arterial hemodynamics (1.8-fold increase in HAVR and 38% decrease in 
      HABF). Post-LPS, HABF 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 HABF 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. Portal hypertension did not 
      occur in iloprost-treated animals, as portal venous pressure remained within 
      baseline range (P < 0.05 vs. nontreated group, ANOVA). Burn and endotoxemia 
      resulted in a significant decrease of hepatic oxygen delivery (hDO2, 63% and 12% 
      of baseline, respectively) and hepatic oxygen 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 prostacyclin treatment appears to have no 
      beneficial effects on hepatic perfusion early postburn. However, during the late 
      postburn endotoxic phase, prostacyclin seems to significantly improve hepatic 
      total blood flow and oxygenation. In addition, prostacyclin treatment attenuated 
      burn- and endotoxin-induced portal hypertension.
FAU - Tadros, Tamer
AU  - Tadros T
AD  - Shriners Burns Institute and the University of Texas Medical Branch, Galveston, 
      TX, USA. t.tadros@erasmusmc.nl
FAU - Traber, Daniel L
AU  - Traber DL
FAU - Herndon, David N
AU  - Herndon DN
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - Ann Surg
JT  - Annals of surgery
JID - 0372354
RN  - DCR9Z582X0 (Epoprostenol)
SB  - IM
MH  - Animals
MH  - Burns/complications/*drug therapy
MH  - Disease Models, Animal
MH  - Epoprostenol/adverse effects/*pharmacology
MH  - Female
MH  - Hypertension, Portal/*drug therapy/etiology
MH  - Liver Circulation/*drug effects/physiology
MH  - Oxygen Consumption/*drug effects/physiology
MH  - Random Allocation
MH  - Reference Values
MH  - Risk Factors
MH  - Sensitivity and Specificity
MH  - Sepsis/complications/*drug therapy
MH  - Severity of Illness Index
MH  - Swine
MH  - Vascular Resistance/drug effects
PMC - PMC1356194
EDAT- 2003/12/20 05:00
MHDA- 2004/01/24 05:00
PMCR- 2004/07/01
CRDT- 2003/12/20 05:00
PHST- 2003/12/20 05:00 [pubmed]
PHST- 2004/01/24 05:00 [medline]
PHST- 2003/12/20 05:00 [entrez]
PHST- 2004/07/01 00:00 [pmc-release]
AID - 0000658-200401000-00010 [pii]
AID - 10.1097/01.sla.0000103073.65311.c8 [doi]
PST - ppublish
SO  - Ann Surg. 2004 Jan;239(1):67-74. doi: 10.1097/01.sla.0000103073.65311.c8.