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Article: Selective versus non-selective suppression of nitric oxide synthase on regional hemodynamics in rats with or without LPS-induced endotoxemia

TitleSelective versus non-selective suppression of nitric oxide synthase on regional hemodynamics in rats with or without LPS-induced endotoxemia
Authors
Issue Date2003
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00210/index.htm
Citation
Naunyn-Schmiedeberg's Archives Of Pharmacology, 2003, v. 367 n. 4, p. 372-379 How to Cite?
AbstractThe late phase of severe septic shock is associated with reduced cardiac output (CO) and activation of the inducible isoform of nitric oxide synthase (NOS). This study examined the effects of 1400 W (N-3-aminomethylbenzyl-acetamidine), a new selective inhibitor of inducible NOS (iNOS), relative to those of NG-nitro-L-arginine (L-NNA, non-selective inhibitor of NOS) and the vehicle, on mean arterial pressure (MAP), CO, total peripheral resistance (TPR) and tissue blood flow (BF) in thiobutabarbital-anesthetized rats with lipopolysaccharide (LPS, 10 mg/kg, i.v.) induced endotoxemia. At 2.5 as well as 4h after injection of LPS, MAP, CO, and BF of the stomach, skeletal muscle and skin were decreased, but TPR was increased, BF to the heart and kidneys were also decreased at 4 h after injection of LPS. Treatment of endotoxemic rats with 1400W (3 mg/kg followed by 3 mg/kg/h, i.v.) at 2.5 h after endotoxin challenge prevented the late phase fall in MAP without exacerbating the decreases in CO and tissue BF. In contrast, treatment with L-NNA (8mg/kg followed by 3 mg/kg/h, i.v.) at 2.5 h did not prevent the decline in MAP in the LPS-treated rats. Furthermore, CO drastically decreased, TPR markedly increased, and BF to the heart, brain, intestine and skeletal muscle were decreased at 4 h relative to the readings in saline- or 1400 W-treated endotoxemic rats. Therefore, selective inhibition of iNOS by 1400 W restores MAP without compromising CO, but non-selective inhibition of NOS is detrimental at the late stage of septic shock.
Persistent Identifierhttp://hdl.handle.net/10722/171297
ISSN
2015 Impact Factor: 2.376
2015 SCImago Journal Rankings: 0.859
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheng, Xen_US
dc.contributor.authorLeung, SWSen_US
dc.contributor.authorLo, LSen_US
dc.contributor.authorPang, CCYen_US
dc.date.accessioned2012-10-30T06:13:14Z-
dc.date.available2012-10-30T06:13:14Z-
dc.date.issued2003en_US
dc.identifier.citationNaunyn-Schmiedeberg's Archives Of Pharmacology, 2003, v. 367 n. 4, p. 372-379en_US
dc.identifier.issn0028-1298en_US
dc.identifier.urihttp://hdl.handle.net/10722/171297-
dc.description.abstractThe late phase of severe septic shock is associated with reduced cardiac output (CO) and activation of the inducible isoform of nitric oxide synthase (NOS). This study examined the effects of 1400 W (N-3-aminomethylbenzyl-acetamidine), a new selective inhibitor of inducible NOS (iNOS), relative to those of NG-nitro-L-arginine (L-NNA, non-selective inhibitor of NOS) and the vehicle, on mean arterial pressure (MAP), CO, total peripheral resistance (TPR) and tissue blood flow (BF) in thiobutabarbital-anesthetized rats with lipopolysaccharide (LPS, 10 mg/kg, i.v.) induced endotoxemia. At 2.5 as well as 4h after injection of LPS, MAP, CO, and BF of the stomach, skeletal muscle and skin were decreased, but TPR was increased, BF to the heart and kidneys were also decreased at 4 h after injection of LPS. Treatment of endotoxemic rats with 1400W (3 mg/kg followed by 3 mg/kg/h, i.v.) at 2.5 h after endotoxin challenge prevented the late phase fall in MAP without exacerbating the decreases in CO and tissue BF. In contrast, treatment with L-NNA (8mg/kg followed by 3 mg/kg/h, i.v.) at 2.5 h did not prevent the decline in MAP in the LPS-treated rats. Furthermore, CO drastically decreased, TPR markedly increased, and BF to the heart, brain, intestine and skeletal muscle were decreased at 4 h relative to the readings in saline- or 1400 W-treated endotoxemic rats. Therefore, selective inhibition of iNOS by 1400 W restores MAP without compromising CO, but non-selective inhibition of NOS is detrimental at the late stage of septic shock.en_US
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00210/index.htmen_US
dc.relation.ispartofNaunyn-Schmiedeberg's Archives of Pharmacologyen_US
dc.subject.meshAmidines - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBenzylamines - Pharmacologyen_US
dc.subject.meshBlood Pressure - Drug Effectsen_US
dc.subject.meshCardiac Output - Drug Effectsen_US
dc.subject.meshEndotoxemia - Chemically Induced - Enzymology - Physiopathologyen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshEscherichia Colien_US
dc.subject.meshHeart Rate - Drug Effectsen_US
dc.subject.meshHemodynamics - Drug Effectsen_US
dc.subject.meshLipopolysaccharidesen_US
dc.subject.meshMaleen_US
dc.subject.meshNitric Oxide Synthase - Antagonists & Inhibitorsen_US
dc.subject.meshNitric Oxide Synthase Type Iien_US
dc.subject.meshNitroarginine - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshRegional Blood Flow - Drug Effectsen_US
dc.subject.meshTime Factorsen_US
dc.titleSelective versus non-selective suppression of nitric oxide synthase on regional hemodynamics in rats with or without LPS-induced endotoxemiaen_US
dc.typeArticleen_US
dc.identifier.emailLeung, SWS:swsleung@hku.hken_US
dc.identifier.authorityLeung, SWS=rp00235en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s00210-002-0684-1en_US
dc.identifier.pmid12690429-
dc.identifier.scopuseid_2-s2.0-0038070302en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0038070302&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume367en_US
dc.identifier.issue4en_US
dc.identifier.spage372en_US
dc.identifier.epage379en_US
dc.identifier.isiWOS:000182947600006-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridCheng, X=37044433300en_US
dc.identifier.scopusauthoridLeung, SWS=24540419500en_US
dc.identifier.scopusauthoridLo, LS=36797964000en_US
dc.identifier.scopusauthoridPang, CCY=7201425219en_US

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