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Titolo:
Roles of IL-1 and TNF in the decreased ileal muscle contractility induced by lipopolysaccharide
Autore:
Lodato, RF; Khan, AR; Zembowicz, MJ; Weisbrodt, NW; Pressley, TA; Li, YF; Lodato, JA; Zembowicz, A; Moody, FG;
Indirizzi:
UnivaTexas, Hlth Sci Ctr, Dept Internal Med, Div Pulm & Crit Care Med,Traum Univ Texas Houston TX USA 77030 ernal Med, Div Pulm & Crit Care Med,Traum Univ7030as, Hlth Sci Ctr, Dept Integrat Biol, Trauma Res Ctr, Houston, TX 7 Univ Texas Houston TX USA 77030 egrat Biol, Trauma Res Ctr, Houston, TX 7 Univ Texas, Hlth Sci Ctr, Dept Surg, Trauma Res Ctr, Houston, TX 77030 USAUniv Texas Houston TX USA 77030 rg, Trauma Res Ctr, Houston, TX 77030 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
fascicolo: 6, volume: 39, anno: 1999,
pagine: G1356 - G1362
SICI:
0193-1857(199906)39:6<G1356:ROIATI>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; NITRIC-OXIDE SYNTHASE; INTERLEUKIN-1 RECEPTOR ANTAGONIST; VASCULAR SMOOTH-MUSCLE; METHYL-L-ARGININE; SEPTIC SHOCK; BACTERIAL TRANSLOCATION; FUSION PROTEIN; ENDOTOXIN; HYPOTENSION;
Keywords:
tumor necrosis factor; interleukin-1; tumor necrosis factor binding protein; interleukin-1 receptor antagonist; soluble tumor necrosis factor receptors; sepsis; nitric oxide; inducible nitric oxide synthase; nitric oxide synthase activity; intestinal transit; endotoxin; ileal smooth muscle;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Lodato, RF UnivaTexas, Hlth Sci Ctr, Dept Internal Med, Div Pulm & Crit Care Med,Traum Univ Texas 6431 Fannin St,Suite 1-274 Houston TX USA 77030 raum
Citazione:
R.F. Lodato et al., "Roles of IL-1 and TNF in the decreased ileal muscle contractility induced by lipopolysaccharide", AM J P-GAST, 39(6), 1999, pp. G1356-G1362

Abstract

Gastrointestinal stasis during sepsis may be associated with gastrointestinal smooth muscle dysfunction. Endotoxin [lipopolysaccharide (LPS)] impairssmooth muscle contraction, in part through inducible nitric oxide synthase(NOS II) and enhanced nitric oxide production. We studied the roles of tumor necrosis factor-alpha (TNF) and interleukin-1 (IL-1) in this process by using TNF binding protein (TNFbp) and IL-1 receptor antagonist (IL-1ra). Rats were treated with TNFbp and IL-1ra, or their vehicles, 1 h before receiving LPS or saline. At 5 h after LPS, contractility was measured in strips of ileal longitudinal smooth muscle, and NOS II activity was measured in full-thickness segments of ileum. LPS decreased maximum stress (mean +/- SE) from 508 +/- 55 (control) to 355 +/- 33 g/cm(2) (P < 0.05). Pretreatment with TNFbp plus IL-1ra prevented the LPS-induced decrease. Separate studies ofTNFbp alone or IL-1ra alone indicated that, at the doses and timing used, TNFbp was more effective. LPS also increased NOS II activity by >10-fold (P< 0.01) over control. This increase was prevented by TNFbp plus IL-1ra (P = not significant vs, control). We conclude that the LPS-induced increase in NOS II activity and the decrease in ileal muscle contractility are mediated by TNF and IL-1.

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Documento generato il 29/11/20 alle ore 14:38:53