Document Detail


Adequacy of gut oxygenation in endotoxemia and sepsis.
MedLine Citation:
PMID:  8428495     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To provide a succinct overview of current notions regarding sepsis-induced alterations in mesenteric perfusion and oxygen transport. DATA SOURCES: Selected English-language articles dealing with mesenteric perfusion and gut mucosal function during sepsis or endotoxicosis in experimental animals or man. STUDY SELECTION AND DATA EXTRACTION: The review emphasizes findings obtained using a well-characterized porcine model of acute, resuscitated endotoxicosis. Other experimental and clinical studies are discussed as well. DATA SYNTHESIS: Total hepatosplanchnic perfusion and oxygen uptake are increased in most patients with compensated sepsis. No data are currently available from clinical studies regarding the effect of sepsis on mesenteric perfusion per se. Data are unavailable regarding either total hepatosplanchnic or mesenteric blood flow in patients with decompensated sepsis (i.e., septic shock). Therefore, current ideas regarding mesenteric perfusion in sepsis derive primarily from studies using animal models. In a normodynamic porcine endotoxicosis model, mesenteric perfusion and oxygen delivery (DO2) are markedly decreased. The changes in flow and DO2 are accompanied by intestinal mucosal acidosis and increased permeability to hydrophilic solutes, suggesting that these latter phenomena are a consequence of lipopolysaccharide-induced mesenteric hypoperfusion. This idea is supported by the observation that maintenance of normal mesenteric blood flow ameliorates gut mucosal acidosis and hyperpermeability in endotoxic pigs. However, because transmesenteric oxygen consumption is unchanged in endotoxic pigs, the precise mechanistic relationship between hypoperfusion and altered barrier function remains puzzling. CONCLUSION: Mesenteric hypoperfusion may be an important factor leading to alterations in gut epithelial permeability in endotoxicosis and sepsis.
Authors:
M P Fink
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Critical care medicine     Volume:  21     ISSN:  0090-3493     ISO Abbreviation:  Crit. Care Med.     Publication Date:  1993 Feb 
Date Detail:
Created Date:  1993-03-08     Completed Date:  1993-03-08     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0355501     Medline TA:  Crit Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  S4-8     Citation Subset:  AIM; IM    
Affiliation:
Department of Surgery, University of Massachusetts Medical Center, Worcester.
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MeSH Terms
Descriptor/Qualifier:
Animals
Disease Models, Animal
Endotoxins
Intestinal Mucosa / physiopathology
Intestines / physiopathology*
Oxygen Consumption*
Sepsis / physiopathology*
Shock, Septic / physiopathology
Splanchnic Circulation*
Swine
Grant Support
ID/Acronym/Agency:
R29 GM3761-05/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Endotoxins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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