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

We investigated the role of the nitric oxide (NO) synthase (NOS) pathway in muscular metabolism during endotoxemia in four groups of male Wister 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 methyleste r ([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 r ats were fed by controlled enteral nutrition and killed on day 3. The resul ts showed that (1) NOS inhibition was detrimental during endotoxemia, incre asing lethality from 20% to 80.5%, and (2) NOS inhibition did not modify th e hypercatabolic state consecutive to endotoxemia, particularly at the musc ular level (nitrogen balance, total-body and muscular weight loss, and musc ular protein and glutamine concentrations). However, myofibrillar catabolis m was delayed in the LPS-NAME group. In conclusion, NO production is of maj or importance for survival after an endotoxemic challenge, but contributes weakly to the metabolic response of muscle to injury. Copyright (C) 1999 by W.B. Saunders Company.