Nitric Oxide May Upregulate In Vivo Hepatic Protein Synthesis During Endotoxemia

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

Research output: Contribution to journalArticle

54 Citations (Scopus)

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 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.

Original languageEnglish
Pages (from-to)152-157
Number of pages6
JournalArchives of Surgery
Volume128
Issue number2
DOIs
Publication statusPublished - 01-01-1993

Fingerprint

Endotoxemia
Nitric Oxide
Up-Regulation
Nitroarginine
Liver
Proteins
Aspartate Aminotransferases
Nitrites
Endotoxins
Nitric Oxide Synthase
Nitrates
Hepatocytes
Hemodynamics
Inflammation
Serum

All Science Journal Classification (ASJC) codes

  • Surgery

Cite this

Frederick, J. A. ; Hasselgren, P. O. ; Davis, S. ; Higashiguchi, Takashi ; Jacob, T. D. ; Fischer, J. E. / Nitric Oxide May Upregulate In Vivo Hepatic Protein Synthesis During Endotoxemia. In: Archives of Surgery. 1993 ; Vol. 128, No. 2. pp. 152-157.
@article{d3dbfe8a4c204ba09aa74d974ef5a117,
title = "Nitric Oxide May Upregulate In Vivo Hepatic Protein Synthesis During Endotoxemia",
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 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.",
author = "Frederick, {J. A.} and Hasselgren, {P. O.} and S. Davis and Takashi Higashiguchi and Jacob, {T. D.} and Fischer, {J. E.}",
year = "1993",
month = "1",
day = "1",
doi = "10.1001/archsurg.1993.01420140029005",
language = "English",
volume = "128",
pages = "152--157",
journal = "JAMA Surgery",
issn = "2168-6254",
publisher = "American Medical Association",
number = "2",

}

Nitric Oxide May Upregulate In Vivo Hepatic Protein Synthesis During Endotoxemia. / Frederick, J. A.; Hasselgren, P. O.; Davis, S.; Higashiguchi, Takashi; Jacob, T. D.; Fischer, J. E.

In: Archives of Surgery, Vol. 128, No. 2, 01.01.1993, p. 152-157.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Nitric Oxide May Upregulate In Vivo Hepatic Protein Synthesis During Endotoxemia

AU - Frederick, J. A.

AU - Hasselgren, P. O.

AU - Davis, S.

AU - Higashiguchi, Takashi

AU - Jacob, T. D.

AU - Fischer, J. E.

PY - 1993/1/1

Y1 - 1993/1/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0027404501&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027404501&partnerID=8YFLogxK

U2 - 10.1001/archsurg.1993.01420140029005

DO - 10.1001/archsurg.1993.01420140029005

M3 - Article

VL - 128

SP - 152

EP - 157

JO - JAMA Surgery

JF - JAMA Surgery

SN - 2168-6254

IS - 2

ER -