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pubmed-article:12434606rdf:typepubmed:Citationlld:pubmed
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pubmed-article:12434606pubmed:dateCreated2002-11-18lld:pubmed
pubmed-article:12434606pubmed:abstractTextHemorrhagic shock upregulates inducible nitric oxide (NO) synthase (iNOS) expression and the resultant NO overproduction. Liver is one of the major organs that is responsible for increased NO production after trauma-hemorrhage and resuscitation. Guanosine triphosphate cyclohydrolase I (GTPCH) is the rate-limiting enzyme for the synthesis of tetrahydrobiopterin (BH4), a necessary co-factor for iNOS activity. Very little is known about the effects of hemorrhagic shock on hepatic GTPCH expression.lld:pubmed
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pubmed-article:12434606pubmed:statusMEDLINElld:pubmed
pubmed-article:12434606pubmed:authorpubmed-author:HuangChun-Jen...lld:pubmed
pubmed-article:12434606pubmed:authorpubmed-author:SkimmingJeffr...lld:pubmed
pubmed-article:12434606pubmed:authorpubmed-author:TsaiPeishanPlld:pubmed
pubmed-article:12434606pubmed:authorpubmed-author:ChengChing-Ro...lld:pubmed
pubmed-article:12434606pubmed:authorpubmed-author:LuYen-TaYTlld:pubmed
pubmed-article:12434606pubmed:authorpubmed-author:HsuYung-WeiYWlld:pubmed
pubmed-article:12434606pubmed:authorpubmed-author:SuNuan-YenNYlld:pubmed
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pubmed-article:12434606pubmed:pagination109-16lld:pubmed
pubmed-article:12434606pubmed:dateRevised2006-11-15lld:pubmed
pubmed-article:12434606pubmed:articleTitleGTPCH is not a rate-limiting factor for hemorrhagic shock-induced hepatic nitric oxide biosynthesis.lld:pubmed
pubmed-article:12434606pubmed:affiliationDepartment of Anesthesiology, Mackay Memorial Hospital, Mackay Junior College of Nursing, Taipei, Taiwan. R.O.C.lld:pubmed