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J. A. Frederick, MD; P. O. Hasselgren, MD; S. Davis, MD; T. Higashiguchi, MD; T. D. Jacob, MD; J. E. Fischer, MD

Arch Surg. 1993;128(2):152-157.

Abstract
• 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 N^G-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 N^G-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 N^G-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.

(Arch Surg. 1993;128:152-157)

Author Affiliations
From the Departments of Surgery (Drs Frederick, Hasselgren, Higashiguchi, and Fischer) and Pathology (Dr Davis), University of Cincinnati (Ohio), and the Department of Surgery, University of Pittsburgh (Pa) (Dr Jacob).

Footnotes
Accepted for publication August 15, 1992.

Presented at the 12th Annual Meeting of the Surgical Infection Society, Los Angeles, Calif, April 10, 1992.

Reprint requests to the Department of Surgery, University of Cincinnati Medical Center, 231 Bethesda Ave, Cincinnati, OH 45267-0558 (Dr Hasselgren).

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