Linked Life Data

8087583

Source:http://linkedlifedata.com/resource/pubmed/id/8087583

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1994-10-20
pubmed:abstractText
In 1987, nitric oxide was reported to be an endothelium-dependent relaxing factor. When inhaled as a gas at low levels, nitric oxide selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because nitric oxide is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled nitric oxide produces local vasodilation of well-ventilated lung units and may "steal" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. In patients with adult respiratory distress syndrome, inhaled nitric oxide reduces pulmonary hypertension and improves arterial oxygenation without reducing systemic arterial pressure. Tachyphylaxis to nitric oxide inhalation has not been observed. While additional chronic toxicology studies need to be performed, significant pulmonary toxicity has not been observed at low inhaled concentrations (< 80 parts per million by volume). Potentially, inhaled nitric oxide may be a valuable therapy in patients with adult respiratory distress syndrome.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1063-7389
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
638-50
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Inhaled nitric oxide in the adult respiratory distress syndrome and other lung diseases.
pubmed:affiliation
Department of Anesthesia, Massachusetts General Hospital, Boston, MA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review