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Titolo:
DIFFERENTIAL-EFFECTS OF NITRIC-OXIDE SYNTHASE INHIBITORS ON ENDOTOXIN-INDUCED LIVER-DAMAGE IN RATS
Autore:
VOS TA; GOUW ASH; KLOK PA; HAVINGA R; VANGOOR H; HUITEMA S; ROELOFSEN H; KUIPERS F; JANSEN PLM; MOSHAGE H;
Indirizzi:
UNIV GRONINGEN HOSP,DIV GASTROENTEROL & HEPATOL,DEPT INTERNAL MED,GRONINGEN INST DRUG STUDIES NL-9700 RB GRONINGEN NETHERLANDS UNIV GRONINGEN HOSP,DEPT PATHOL NL-9700 RB GRONINGEN NETHERLANDS UNIV GRONINGEN HOSP,DEPT PEDIAT NL-9700 RB GRONINGEN NETHERLANDS
Titolo Testata:
Gastroenterology
fascicolo: 4, volume: 113, anno: 1997,
pagine: 1323 - 1333
SICI:
0016-5085(1997)113:4<1323:DONSIO>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
SELECTIVE-INHIBITION; PERFUSED LIVER; L-ARGININE; SHOCK; HEPATOCYTES; POTENT; MICE; LOCALIZATION; RESPONSES; CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
54
Recensione:
Indirizzi per estratti:
Citazione:
T.A. Vos et al., "DIFFERENTIAL-EFFECTS OF NITRIC-OXIDE SYNTHASE INHIBITORS ON ENDOTOXIN-INDUCED LIVER-DAMAGE IN RATS", Gastroenterology, 113(4), 1997, pp. 1323-1333

Abstract

Background & Aims: During endotoxemia, expression of inducible nitricoxide synthase (iNOS) and nitric oxide production in the liver is increased, NO has been suggested to have a hepatoprotective function. Theaim of this study was to investigate the distribution of iNOS and theeffect of different NO synthase inhibitors on liver damage and hemodynamics during endotoxemia. Methods: Rats were injected with lipopolysaccharide (LPS) and received the NOS-inhibitor S-methylisothiourea (SMT) or NG-nitro-L-arginine methyl ester (L-NAME). iNOS induction was assessed by Western blot, immunohistochemistry, and measurement of NO metabolites in plasma and bile. Liver damage was determined by aspartate aminotransferase and alanine aminotransferase and by histology. The effects of both inhibitors on systemic and portal pressure were measuredin normal and LPS-treated rats. Results: LPS treatment strongly induced iNOS in inflammatory cells, macrophages, bile duct epithelium, and hepatocytes, especially at the canalicular membrane, LPS-induced liverdamage strongly increased after L-NAME. SMT caused a similar reduction of NO production without enhancing liver damage. In LPS-treated rats, SMT increased the systemic and portal pressure significantly more than L-NAME. Conclusions: During endotoxemia, administration of the NOS-inhibitor L-NAME aggravates liver damage. This liver damage does not seem to be caused by hemodynamic changes, In contrast, SMT caused significant hemodynamic changes but did not increase LPS-induced liver damage.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 13:05:05