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Titolo:
PNEUMOTOXICITY OF LIPOPOLYSACCHARIDE IN NITRIC-OXIDE - DEFICIENT RATSIS LIMITED BY A THROMBOXANE SYNTHASE INHIBITOR
Autore:
WOLKOW PP; BARTUS JB; GRYGLEWSKI RJ;
Indirizzi:
JAGIELLONIAN UNIV,COLL MED,CHAIR PHARMACOL,DEPT PHARMACOL,GRZEGORZECKA 16 PL-31531 KRAKOW POLAND JAGIELLONIAN UNIV,COLL MED,CHAIR PHARMACOL,DEPT PHARMACOL PL-31531 KRAKOW POLAND
Titolo Testata:
Journal of Physiology and Pharmacology
fascicolo: 4, volume: 48, anno: 1997,
pagine: 645 - 653
SICI:
0867-5910(1997)48:4<645:POLIN->2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
NECROSIS-FACTOR-ALPHA; COLI SEPTIC SHOCK; SEPSIS SYNDROME; DOUBLE-BLIND; L-ARGININE; ENDOTOXIN; PROSTACYCLIN; ANTIBODY; FAILURE; HYPOTENSION;
Keywords:
LUNG INJURY; NITRIC OXIDE; THROMBOXANE; PROSTACYCLIN; LIPOPOLYSACCHARIDE;
Tipo documento:
Article
Natura:
Periodico
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
P.P. Wolkow et al., "PNEUMOTOXICITY OF LIPOPOLYSACCHARIDE IN NITRIC-OXIDE - DEFICIENT RATSIS LIMITED BY A THROMBOXANE SYNTHASE INHIBITOR", Journal of Physiology and Pharmacology, 48(4), 1997, pp. 645-653

Abstract

Both nitric oxide and arachidonic acid metabolites have been implicated in pathogenesis of septic shock. We have recently described a modelof endotoxin-induced acute lung injury in rats in which nitric oxide synthase is inhibited. The possible interplay between nitric oxide andeicosanoids (thromboxane A(2), prostacyclin) in this model have been presently studied. Animals were randomly assigned to four experimentalgroups which received the following treatment. 1. Lipopolysaccharide (LPS) infusion only, 2 mg.kg(-1)min(-1) during 10 min (LPS group). 2. N-omega-Nitro-L-Arginine 10 mg.kg(-1) (L-NNA, nitric oxide synthase inhibitor) pretreatment followed by LPS infusion (L-NNA+LPS group). 3. L-NNA and camonagrel 25 mg.kg(-1) (CAM, thromboxane synthase inhibitor)pretreatment followed by LPS infusion (L-NNA+CAM+LPS group). 4. L-NNAand iloprost 0.3 mu g.kg(-1).min(-1)(ILO, stable analog of prostacyclin) pretreatment followed by LPS infusion (L-NNA+ILO+LPS group). LPS infusion resulted in a biphasic response in mean arterial blood pressure. A transient but deep fall in arterial blood pressure was followed by a long-lasting hypotension that led to death after 278 +/- 49 min. L-NNA+LPS rats died within 22+/-5 min among the symptoms of systemic hypotension and acute lung injury. In L-NNA+CAM+LPS group a significant attenuation of early phase of hypotension occured and survival time was comparable with that of the LPS group (298+/-68 min). In rats of theL-NNA+ILO+LPS group survival time increased Insignificantly to 48+/-41 min. It is concluded that immediate deleterious effects of lipopolysaccharide in NO-deficient rats are at least partially mediated by thromboxane A(2) while prostacyclin cannot replace NO in its pneumoprotective action.

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Documento generato il 20/09/20 alle ore 01:06:22