Affordable Access

Is the L-arginine-nitric oxide pathway involved in endotoxemia-induced muscular hypercatabolism in rats?

Authors
  • Pernet, P
  • Coudray-Lucas, C
  • Le Boucher, J
  • Schlegel, L
  • Giboudeau, J
  • Cynober, L
  • Aussel, C
Type
Published Article
Journal
Metabolism
Publisher
Elsevier
Publication Date
Feb 01, 1999
Volume
48
Issue
2
Pages
190–193
Identifiers
PMID: 10024080
Source
Medline
License
Unknown

Abstract

We investigated the role of the nitric oxide (NO) synthase (NOS) pathway in muscular metabolism during endotoxemia in four groups of male Wistar rats. Two groups were injected with the lipopolysaccharide (LPS) of Escherichia coli (3 mg/kg), with one group treated using N(G)-nitro-L-arginine methylester ([L-NAME] 85 mg/kg/d) and the other not. The two control groups included one treated with L-NAME and the other not. After 24 hours of fasting, the rats were fed by controlled enteral nutrition and killed on day 3. The results showed that (1) NOS inhibition was detrimental during endotoxemia, increasing lethality from 20% to 80.5%, and (2) NOS inhibition did not modify the hypercatabolic state consecutive to endotoxemia, particularly at the muscular level (nitrogen balance, total-body and muscular weight loss, and muscular protein and glutamine concentrations). However, myofibrillar catabolism was delayed in the LPS-NAME group. In conclusion, NO production is of major importance for survival after an endotoxemic challenge, but contributes weakly to the metabolic response of muscle to injury.

Report this publication

Statistics

Seen <100 times