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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2003-9-12
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pubmed:abstractText |
Increased pulmonary vascular resistance (PVR) because of congenital heart disease (CHD) may be caused by a dysfunction in endogenous pulmonary endothelial nitric oxide (NO) production. In other forms of pulmonary vascular disease with increased PVR, an elevated activity of a phosphodiesterase type 5 (PDE-5), responsible for the degradation of cyclic guanidine monophosphate (cGMP), the second messenger of endothelially produced NO, has been demonstrated. This study compares the effects of inhaled NO before and after the specific inhibition of the PDE-5 by intravenous sildenafil (Viagra) in pre- and postoperative children with increased PVR because of CHD.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/3',5'-Cyclic-GMP Phosphodiesterases,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic Nucleotide...,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/PDE5A protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphodiesterase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Piperazines,
http://linkedlifedata.com/resource/pubmed/chemical/Purines,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfones,
http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents,
http://linkedlifedata.com/resource/pubmed/chemical/sildenafil
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1524-4539
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
9
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pubmed:volume |
108 Suppl 1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
II167-73
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:12970227-3',5'-Cyclic-GMP Phosphodiesterases,
pubmed-meshheading:12970227-Administration, Inhalation,
pubmed-meshheading:12970227-Adolescent,
pubmed-meshheading:12970227-Blood Pressure,
pubmed-meshheading:12970227-Child,
pubmed-meshheading:12970227-Child, Preschool,
pubmed-meshheading:12970227-Combined Modality Therapy,
pubmed-meshheading:12970227-Cyclic GMP,
pubmed-meshheading:12970227-Cyclic Nucleotide Phosphodiesterases, Type 5,
pubmed-meshheading:12970227-Heart Catheterization,
pubmed-meshheading:12970227-Heart Defects, Congenital,
pubmed-meshheading:12970227-Hemodynamics,
pubmed-meshheading:12970227-Humans,
pubmed-meshheading:12970227-Infant,
pubmed-meshheading:12970227-Infusions, Intravenous,
pubmed-meshheading:12970227-Nitric Oxide,
pubmed-meshheading:12970227-Phosphodiesterase Inhibitors,
pubmed-meshheading:12970227-Piperazines,
pubmed-meshheading:12970227-Postoperative Period,
pubmed-meshheading:12970227-Pulmonary Artery,
pubmed-meshheading:12970227-Pulmonary Circulation,
pubmed-meshheading:12970227-Purines,
pubmed-meshheading:12970227-Sulfones,
pubmed-meshheading:12970227-Vascular Resistance,
pubmed-meshheading:12970227-Vasodilator Agents
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pubmed:year |
2003
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pubmed:articleTitle |
Intravenous sildenafil is a potent pulmonary vasodilator in children with congenital heart disease.
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pubmed:affiliation |
Abteilung für Angeborene Herzfehler, Deutsches Herzzentrum Berlin, Berlin, Germany.
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Comparative Study,
Controlled Clinical Trial,
Research Support, Non-U.S. Gov't
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