Document Detail

Carnitine deprivation adversely affects cardiac performance in the lipopolysaccharide- and hypoxia/reoxygenation-stressed piglet heart.
MedLine Citation:
PMID:  10030799     Owner:  NLM     Status:  MEDLINE    
Sepsis and hypoxia are important stressors for the neonate. Newborn infants receiving total parenteral nutrition are routinely deprived of carnitine and develop low carnitine plasma and tissue levels. Because of its high metabolic rate and dependence on fatty acids for energy, the newborn heart may be particularly vulnerable to stress in the face of an inadequate carnitine supply. To investigate whether carnitine deprivation affects cardiac performance under stress, 23 neonatal piglets received parenteral nutrition for 2-3 weeks that was either carnitine free (CARN -) or supplemented (CARN +) with L-carnitine (400 mg/L). Bacterial endotoxin (lipopolysaccharide (LPS), 250 microg/kg intravenous bolus) or saline vehicle was administered to anesthetized piglets 3 h prior to study of isolated perfused hearts. Left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure, and left ventricular developed pressure (LVDP) were measured in vitro under aerobic, hypoxic, and reoxygenation conditions in all animals. Plasma and tissue carnitine values were lower in CARN - than in CARN + piglets. In hearts from LPS-treated animals prior to hypoxia, there was no difference in ventricular compliance between CARN - and CARN + groups. LVSP and LVDP were lower in CARN - than CARN + hearts. During hypoxia, LVSP and LVDP fell, but left ventricular end diastolic pressure increased in hearts from both LPS- and saline- treated piglets. Reoxygenation led to poorer recovery in CARN - than CARN + hearts from LPS-treated animals, but not from saline controls. During hypoxia/reoxygenation, lactate efflux initially rose and then fell, while carnitine efflux increased continually. Acetyl- and medium-chain acylcarnitines were detected in the coronary effluent. Our findings suggest that carnitine deprivation diminishes heart carnitine concentrations and impairs cardiac recovery from combined endotoxic and hypoxic stress. Possible mechanisms include reduced acyl buffering and/or impaired transport of fatty acyl groups into mitochondria.
D Penn; L Zhang; P J Bobrowski; M Quinn; K H McDonough
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  11     ISSN:  1073-2322     ISO Abbreviation:  Shock     Publication Date:  1999 Feb 
Date Detail:
Created Date:  1999-04-28     Completed Date:  1999-04-28     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  120-6     Citation Subset:  IM    
Department of Pediatrics, Louisiana State University Medical Center, New Orleans 70112, USA.
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MeSH Terms
Animals, Newborn
Anoxia / metabolism*
Carnitine / deficiency*,  metabolism,  pharmacology
Escherichia coli
Heart / growth & development,  physiopathology*
Heart Rate
Lactates / metabolism
Myocardium / metabolism
Sepsis / chemically induced,  physiopathology*
Stress, Physiological / physiopathology
Ventricular Function, Left
Grant Support
Reg. No./Substance:
0/Lactates; 0/Lipopolysaccharides; 541-15-1/Carnitine

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

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