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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
|
| pubmed:dateCreated |
1997-9-8
|
| pubmed:abstractText |
Nitric oxide (NO) released from endothelium mediates the vasodilatation caused by numerous autacoids. Nitric oxide can also be exogenous in that some drugs used in cardiovascular disease are NO donors (e.g. glyceryl trinitrate, sodium nitroprusside and isosorbide mononitrate used in angina). However, the notion that NO is a cardiac protectant, whose mimicry or supplementation is desirable, has recently been questioned by data that suggest it is an innocent bystander in some conditions, and even a pathological mediator of dysfunction in others. This important issue is discussed by Mike Curtis and Ravinder Pabla who suggest it is necessary to reappraise the role of NO modulation in cardiac pharmacotherapy.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
0165-6147
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
18
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
239-44
|
| pubmed:dateRevised |
2009-9-29
|
| pubmed:meshHeading | |
| pubmed:year |
1997
|
| pubmed:articleTitle |
Nitric oxide supplementation or synthesis block--which is the better approach to treatment of heart disease?
|
| pubmed:affiliation |
Pharmacology Research Laboratoriè, King's College, University of London, UK.
|
| pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
|