Linked Life Data

11751719

Source:http://linkedlifedata.com/resource/pubmed/id/11751719

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-12-25
pubmed:abstractText
Endothelial NO synthase, being deficient in arginine and/or tetrahydrobiopterin, produces in addition to NO a significant concentration of superoxide (O2)(-)). We investigated whether such an imbalance between O2(-) and NO production is present in dysfunctional aortas of Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) with failing hearts after myocardial infarction. Heart failure was induced by permanent occlusion of the left coronary artery, resulting in a large infarction of the free left ventricular wall. Eight weeks after myocardial infarction, when WKY and SHR had compensated heart failure and congestive heart failure, respectively, calcium ionophore-induced NO release (assessed by a NO-sensitive microsensor) from aortic endothelial cells was significantly reduced from 478+/-48 to 216+/-16 nmol/L and 693+/-131 to 257+/-53 nmol/L in WKY and SHR, respectively. Concomitantly, significant increases in calcium ionophore-stimulated O2(-) production (assessed by an electrochemical sensor) could be observed in aortic endothelial cells from infarcted WKY rats (22+/-3.2 versus sham, 10.1+/-1.2 nmol/L) and SHR (102+/-8 versus sham, 67+/-5 nmol/L). A dramatic increase in endothelial peroxynitrite concentration (chemiluminescence method) from 35+/-4 to 90+/-3 nmol/L for WKY and from 60+/-5 to 170+/-10 nmol/L for SHR also was detected. Thus, the markedly decreased NO availability probably caused by impaired endothelial NO synthase activity with enhanced O2(-) and peroxynitrite production appears to be attributable to endothelial dysfunction in normotensive rats with chronic heart failure and especially in hypertensive rats with severe congestive heart failure.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1367-71
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Decreased nitric oxide availability in normotensive and hypertensive rats with failing hearts after myocardial infarction.
pubmed:affiliation
Aventis Pharma Deutschland, DG Cardiovascular Diseases, Frankfurt/Main, Germany.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't