Document Detail


Hepatic and gastrointestinal oxygen and lactate metabolism during low cardiac output in lambs.
MedLine Citation:
PMID:  9167197     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We previously observed young lambs to be more tolerant of hypoxia; compared with older lambs, they accumulate lactate at a slower rate during comparable reduction in cardiac output, and have a greater percent decrease in cardiac output before onset of systemic lactate accumulation. To determine the mechanism of lactic acidosis and the cause for this "tolerance," we reduced cardiac output progressively in seven chronically catheterized conscious lambs (16.4 + 5.1 d) and measured hepatic and gastrointestinal (GI) blood flow (radioactive microspheres) and delivery, uptake, and extraction of lactate and O2. Hepatic O2 consumption declined proportionately below a critical hepatic O2 delivery (approximately 2 mL O2/min/kg), corresponding to the systemic O2 delivery associated with the onset of systemic lactate accumulation. As hepatic O2 delivery decreased below the critical value, there was initially net hepatic lactate uptake and then a change to net production when the O2 delivery decreased below approximately 1 mL O2/min kg. The GI tract had net lactate production at rest, but surprisingly switched to lactate uptake as cardiac output decreased. The mechanism of lactic acidosis was failure of hepatic lactate uptake to increase despite increased hepatic lactate delivery, as reported in adults subjects. However, in contrast, there was "true" hepatic dysfunction and lactate production only at the lowest levels of cardiac output, after onset of systemic lactate accumulation. Moreover, we speculate that tolerance of young lambs to hypoxia is at least due to two factors: 1) hepatic lactate uptake is maintained beyond the "critical" O2 delivery and fall in hepatic O2 consumption, and 2) there is a switch to lactate uptake by the GI tract serving to buffer the lactate.
Authors:
J T Fahey; G Lister; D J Sanfilippo; D I Edelstone
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Pediatric research     Volume:  41     ISSN:  0031-3998     ISO Abbreviation:  Pediatr. Res.     Publication Date:  1997 Jun 
Date Detail:
Created Date:  1997-07-18     Completed Date:  1997-07-18     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0100714     Medline TA:  Pediatr Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  842-51     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut 06520-8064, USA.
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MeSH Terms
Descriptor/Qualifier:
Acidosis, Lactic / metabolism,  physiopathology*
Animals
Cardiac Output, Low / metabolism,  physiopathology*
Digestive System / blood supply,  metabolism*
Lactates / metabolism*
Liver / metabolism*
Liver Circulation
Models, Cardiovascular
Oxygen / blood
Oxygen Consumption*
Regional Blood Flow
Sheep
Grant Support
ID/Acronym/Agency:
HD19092/HD/NICHD NIH HHS; HL07272/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Lactates; 7782-44-7/Oxygen

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


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