Linked Life Data

12902916

Source:http://linkedlifedata.com/resource/pubmed/id/12902916

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2003-8-6
pubmed:abstractText
Recent data suggest that hydroxyurea (HU) increases the production of nitric oxide (NO), a potent vasodilator. NO is normally metabolized from l-Arginine (Arg). However, in vitro and animal experiments suggest that HU is the NO donor itself. In contrast, a recent study indicates that nitric oxide synthase (NOS) may play a role. Since adults with sickle cell disease (SCD) are Arg-deficient, Arg availability may limit the ability of HU to maximally impact NO production if an NOS mechanism is involved. The authors have previously shown that Arg supplementation alone induces a paradoxical decrease in NO metabolite (NO(x)) production.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1077-4114
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
629-34
pubmed:dateRevised
2011-10-6
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Hydroxyurea and arginine therapy: impact on nitric oxide production in sickle cell disease.
pubmed:affiliation
Department of Emergency Medicine, Children's Hospital and Research Center at Oakland, Oakland, California 94609, USA. cmorris@mail.cho.org
pubmed:publicationType
Journal Article, Clinical Trial, Research Support, U.S. Gov't, P.H.S.