Linked Life Data

12016261

Source:http://linkedlifedata.com/resource/pubmed/id/12016261

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2002-5-17
pubmed:abstractText
Transgenic (TG) mice with cardiac-specific overexpression of tumor necrosis factor-alpha develop congestive heart failure. We have previously reported that short-term inhibition of inducible nitric oxide synthase (iNOS) ameliorates beta-adrenergic hyporesponsiveness in TG mice. To examine whether long-term inhibition of iNOS may rescue TG mice from developing congestive heart failure, we disrupted iNOS gene by crossing TG mice with iNOS knockout mice. Myocardial levels of iNOS protein were significantly increased in TG mice compared with age- and sex-matched wild-type (WT) mice. No iNOS protein was detected in TG mice with the disruption of iNOS. Myocardial levels of endothelial NOS were not different among these mice. To examine the effects of iNOS disruption on myocardial contractility, left ventricular pressure was measured. In TG mice, +dP/dt(max) was significantly suppressed, and its beta-adrenergic responsiveness was blunted. As in the case with short-term inhibition of iNOS, the disruption of iNOS gene improved beta-adrenergic inotropic responsiveness in TG mice but not in WT mice. However, the iNOS disruption did not alter myocardial inflammation, ventricular hypertrophy, or the survival of these mice. These results indicate that although myocardial expression of iNOS plays a key role in the attenuation of beta-adrenergic inotropic responsiveness, NO-independent mechanisms might be more important in the development of congestive heart failure.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
17
pubmed:volume
90
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
959-65
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12016261-Adrenergic beta-Agonists, pubmed-meshheading:12016261-Animals, pubmed-meshheading:12016261-Blood Pressure, pubmed-meshheading:12016261-Blotting, Western, pubmed-meshheading:12016261-Cardiomyopathies, pubmed-meshheading:12016261-Enzyme Induction, pubmed-meshheading:12016261-Female, pubmed-meshheading:12016261-Genotype, pubmed-meshheading:12016261-Heart Rate, pubmed-meshheading:12016261-Isoproterenol, pubmed-meshheading:12016261-Male, pubmed-meshheading:12016261-Mice, pubmed-meshheading:12016261-Mice, Inbred C57BL, pubmed-meshheading:12016261-Mice, Knockout, pubmed-meshheading:12016261-Mice, Transgenic, pubmed-meshheading:12016261-Mutation, pubmed-meshheading:12016261-Myocardial Contraction, pubmed-meshheading:12016261-Myocardium, pubmed-meshheading:12016261-Nitric Oxide Synthase, pubmed-meshheading:12016261-Nitric Oxide Synthase Type II, pubmed-meshheading:12016261-Nitric Oxide Synthase Type III, pubmed-meshheading:12016261-Organ Size, pubmed-meshheading:12016261-Survival Analysis, pubmed-meshheading:12016261-Tumor Necrosis Factor-alpha
pubmed:year
2002
pubmed:articleTitle
Disruption of inducible nitric oxide synthase improves beta-adrenergic inotropic responsiveness but not the survival of mice with cytokine-induced cardiomyopathy.
pubmed:affiliation
Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't