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Titolo:
PROTECTIVE ROLE OF PULMONARY NITRIC-OXIDE IN THE ACUTE-PHASE OF ENDOTOXEMIA IN RATS
Autore:
GRYGLEWSKI RJ; WOLKOW PP; URACZ W; JANOWSKA E; BARTUS JB; BALBATUN O; PATTON S; BROVKOVYCH V; MALINSKI T;
Indirizzi:
JAGIELLONIAN UNIV,COLL MED,DEPT PHARMACOL,GRZEGORZECKA 16 PL-31531 KRAKOW POLAND OAKLAND UNIV,DEPT CHEM,INST BIOTECHNOL ROCHESTER MI 48309
Titolo Testata:
Circulation research
fascicolo: 7, volume: 82, anno: 1998,
pagine: 819 - 827
SICI:
0009-7330(1998)82:7<819:PROPNI>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
REQUIRING PROLONGED OBSERVATION; SYNTHASE INHIBITOR; PEROXYNITRITE; THROMBOXANE; SURVIVAL; PATIENT; DESIGN; SHOCK; CELLS; LUNG;
Keywords:
LUNG; MICROCIRCULATION; SHOCK;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
28
Recensione:
Indirizzi per estratti:
Citazione:
R.J. Gryglewski et al., "PROTECTIVE ROLE OF PULMONARY NITRIC-OXIDE IN THE ACUTE-PHASE OF ENDOTOXEMIA IN RATS", Circulation research, 82(7), 1998, pp. 819-827

Abstract

We present for the first time direct continuous assay of NO concentration (porphyricic sensor) in the lung parenchyma of Sprague-Dawley rats in vivo during endotoxemia. Intravenous infusion of lipopolysaccharide (LPS, 2 mg.kg(-1).min(-1) for 10 minutes) stimulated an acute burstof NO from constitutive NO synthase (NOS) that peaked 10 to 15 minutes after the start of LPS infusion, mirroring a coincident peak drop inarterial pressure. NO concentration declined over the next hour to twice above pre-LPS infusion NO levels, where it remained until the ratsdied, 5 to 6 hours after LPS infusion. The chronic drop in arterial pressure observed from 70 minutes to 6 hours after the start of LPS infusion was not convincingly mirrored by a chronic increase in NO concentration, even though indirect NO assay (Griess method, assaying NO decay products NO2-/NO3-) showed that NO production was increasing as a result of continuous NO release by inducible NOS. A NOS inhibitor, N-omega-nitro-L-arginine (L-NNA, 10 mg/kg IV) injected 45 minutes before LPS infusion, resulted in sudden death accompanied by macroscopically/microscopically diagnosed symptoms similar to acute respiratory distress syndrome <25 minutes after the start of LPS infusion. Pharmacological analysis of this L-NNA+LPS model by replacing L-NNA with 1-amino-2-hydroxy-guanidine (selective inhibitor of inducible NOS) or by pretreatment with S-nitroso-N-acetyl-peniciilamine (NO donor), camonagrel (thromboxane synthase inhibitor), or WEB2170 (platelet-activating factor receptor antagonist) indicated that in the early acute phase of endotoxemia, LPS stimulated the production of cytoprotective NO, cytotoxic thromboxane A(2), and platelet-activating factor.

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Documento generato il 28/10/20 alle ore 07:51:40