Nitric oxide may upregulate in vivo hepatic protein synthesis during endotoxemia
J. A. Frederick, P. O. Hasselgren, S. Davis, T. Higashiguchi, T. D. Jacob and J. E. Fischer
Department of Surgery, University of Cincinnati, Ohio.
Nitric oxide (NO) has been implicated as a mediator of hemodynamic and
metabolic changes associated with endotoxemia and inflammation. In vitro
studies suggest that NO inhibits hepatocyte protein synthesis but the role
of NO in the regulation of hepatic protein synthesis in vivo is not known.
In this study, rats were given endotoxin or saline after pretreatment with
the NO synthase inhibitor NG-nitro-L-arginine or solvent, and plasma levels
of nitrite (NO2), nitrate (NO3), and aspartate aminotransferase and hepatic
protein synthesis rate in vivo were measured after 4 and 10 hours. The
NG-nitro-L-arginine effectively blocked the increase in serum NO2/NO3 seen
in endotoxemia and also inhibited the increase in hepatic protein synthesis
in endotoxemic rats. The aspartate aminotransferase levels were elevated in
endotoxemic rats pretreated with NG-nitro-L-arginine. Results support
previous reports of a protective effect of NO on the liver in endotoxemia
and suggest that NO may upregulate hepatic protein synthesis in vivo.
Further study is needed to clarify the reason for the apparent difference
between the effect of NO on hepatic protein synthesis in vivo and in vitro.
