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Titolo:
EFFECT OF L-LYSINE ON NITRIC-OXIDE OVERPRODUCTION IN ENDOTOXIC-SHOCK
Autore:
LIAUDET L; GNAEGI A; ROSSELET A; MARKERT M; BOULAT O; PERRET C; FEIHL F;
Indirizzi:
UNIV LAUSANNE HOSP,INST PATHOPHYSIOL,BH 19-313 CH-1011 LAUSANNE SWITZERLAND UNIV LAUSANNE HOSP,INST PATHOPHYSIOL CH-1011 LAUSANNE SWITZERLAND UNIV LAUSANNE HOSP,CENT LAB CLIN CHEM CH-1011 LAUSANNE SWITZERLAND
Titolo Testata:
British Journal of Pharmacology
fascicolo: 4, volume: 122, anno: 1997,
pagine: 742 - 748
SICI:
0007-1188(1997)122:4<742:EOLONO>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
MULTIPLE ORGAN DYSFUNCTION; CATIONIC AMINO-ACIDS; L-ARGININE TRANSPORT; SEPTIC SHOCK; SELECTIVE INHIBITOR; RODENT MODELS; SYNTHASE; RAT; AMINOGUANIDINE; ENDOTHELIUM;
Keywords:
NITRIC OXIDE; INDUCIBLE NITRIC OXIDE SYNTHASE; ENDOTHELIAL CONSTITUTIVE NITRIC OXIDE SYNTHASE; L-LYSINE; L-ARGININE; SYSTEM Y(+); ENDOTOXIC SHOCK; LIPOPOLYSACCHARIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
L. Liaudet et al., "EFFECT OF L-LYSINE ON NITRIC-OXIDE OVERPRODUCTION IN ENDOTOXIC-SHOCK", British Journal of Pharmacology, 122(4), 1997, pp. 742-748

Abstract

1 An enhanced production of nitric oxide (NO) from L-arginine, related to the diffuse expression of an inducible NO synthase (iNOS), contributes to the pathogenesis of endotoxic shock. Since iNOS activity depends on extracellular L-arginine, we hypothesized that limiting cellular L-arginine uptake would reduce NO production in endotoxic shock. We investigated the effects of L-lysine, an inhibitor of L-arginine uptake through system y(+), on NO production, multiple organ dysfunction and lactate levels, in normal and endotoxaemic rats. 2 Anaesthetized rats challenged with intravenous lipopolysaccharide (LPS, 10 mg kg(-1)) received a 5 h infusion of either L-lysine (500 mu mol kg(-1) h(-1), n=12) or isotonic saline (2 mi kg(-1) h(-1), n=11). In rats treated withsaline, LPS produced a large increase in plasma nitrate and L-citrulline concentrations at 5 h, both markers of enhanced NO production. LPSalso caused severe hypotension, low cardiac output and marked hyperlactataemia. All these changes were significantly reduced by L-lysine administration. 3 Endotoxaemia also caused a significant rise in the plasma levels of alanine aminotransferase (ALAT), lipase, urea and creatinine, and hence, liver, pancreatic and renal dysfunction. These changes tended to be less pronounced in rats treated with L-lysine, althoughthe differences did not reach statistical significance. 4 Similar experiments were conducted in 10 rats challenged with LPS vehicle in place of LPS and then treated with L-lysine (500 mu mol kg(-1) h(-1), n=5)or saline (2 mi kg(-1) h(-1), n=5) for 5 h. In these animals, all thehaemodynamic and metabolic variables remained stable and not statistically different between both treatment groups, except for a slight rise in ALAT, which was comparable in L-lysine and saline-treated rats. 5In conclusion, L-lysine, an inhibitor of cellular L-arginine uptake, reduces NO production and exerts beneficial haemodynamic effects in endotoxaemic rats. L-lysine also reduces hyperlactataemia and tends to blunt the development of organ injury in these animals. Contrastingly, L-lysine has no effects in the absence of endotoxin and thus appears to act as a selective modulator of iNOS activity.

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Documento generato il 05/07/20 alle ore 00:24:57