LPS-induced changes in myocardial markers in neonatal rats

Biol Neonate. 2003;84(4):319-24. doi: 10.1159/000073641.

Abstract

Lipopolysaccharide (LPS) produces varied systemic metabolic effects. We studied the effects of LPS on the cardiac fatty acid profile and its relationship to energy metabolism and inflammatory mediators that included TNF-alpha and nitric oxide synthase (NOS) in 10-day-old neonatal rat pups. Rat pups received an i.p. injection of LPS after a 4-hour starvation period, followed by collection of blood and cardiac tissue 4 h following LPS administration. Compared to controls, LPS induced significant hypoglycemia and hyperlactacidemia, suggesting the development of endotoxic shock. The result was a significant depression in total fatty acid levels as well as non-esterified fatty acid in the cardiac tissue of the LPS-treated pups. In addition, LPS-treated pups also showed a significant increase in TNF-alpha, NOS levels with a depressed redox state and energy metabolism in cardiac tissue. These observations suggest that endotoxic shock in 10-day-old rat pups induces a systemic inflammatory response with a depression in fatty acid metabolism that may contribute to myocardial failure.

MeSH terms

  • Adenosine Triphosphate / analysis
  • Animals
  • Animals, Newborn / metabolism*
  • Biomarkers / analysis*
  • Blood Glucose / metabolism
  • Energy Metabolism / drug effects
  • Fatty Acids / analysis
  • Homeostasis / drug effects
  • Hypoglycemia / chemically induced
  • Lactic Acid / blood
  • Lipopolysaccharides / pharmacology*
  • Myocardium / chemistry*
  • Myocardium / metabolism
  • Nitric Oxide Synthase / analysis
  • Nitric Oxide Synthase Type II
  • Oxidative Stress / drug effects
  • Phosphocreatine / analysis
  • Rats
  • Rats, Sprague-Dawley
  • Salmonella enteritidis
  • Tumor Necrosis Factor-alpha / analysis

Substances

  • Biomarkers
  • Blood Glucose
  • Fatty Acids
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Phosphocreatine
  • Lactic Acid
  • Adenosine Triphosphate
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II
  • Nos2 protein, rat