Linked Life Data

21188246

Source:http://linkedlifedata.com/resource/pubmed/id/21188246

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-12-28
pubmed:abstractText
Reduced nitric oxide (NO) bioavailability and increased oxidative stress are major factors mediating ischemia/reperfusion (I/R) injury. Tetrahydrobiopterin (BH(4)) is an essential cofactor of endothelial NO synthase (eNOS) to produce NO, whereas dihydrobiopterin (BH(2)) can shift the eNOS product profile from NO to superoxide, which is further converted to hydrogen peroxide (H(2)O(2)) and cause I/R injury. The effects of BH(4) and BH(2) on oxidative stress and postreperfused cardiac functions were examined in ex vivo myocardial and in vivo femoral I (20?min)/R (45?min) models. In femoral I/R, BH(4) increased NO and decreased H(2)O(2) releases relative to saline control, and these effects correlated with improved postreperfused cardiac function. By contrast, BH(2) decreased NO release relative to the saline control, but increased H(2)O(2) release similar to the saline control, and these effects correlated with compromised postreperfused cardiac function. In conclusion, these results suggest that promoting eNOS coupling to produce NO and decrease H(2)O(2) may be a key mechanism to restore postreperfused organ function during early reperfusion.
pubmed:language
eng
pubmed:journal
pubmed:status
PubMed-not-MEDLINE
pubmed:issn
1687-6342
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
2010
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
963914
pubmed:year
2010
pubmed:articleTitle
The role of tetrahydrobiopterin and dihydrobiopterin in ischemia/reperfusion injury when given at reperfusion.
pubmed:affiliation
Department of Pathology, Microbiology and Immunology & Forensic Medicine, Philadelphia College of Osteopathic Medicine, 4170 City Avenue, Philadelphia, PA 19131-1694, USA.
pubmed:publicationType
Journal Article