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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-9-7
pubmed:abstractText
The aims of our study were to determine mortality, and age- and genotype-related cardiac phenotype in endothelial nitric oxide synthase (NOS) knockout (-/-) and wild-type (+/+) mice. Male and female (-/-) and male and female (+/+) conscious mice were studied at different ages by echocardiography and tail-cuff blood pressure (BP) measurement. Only 50% male (-/-) mice lived longer than 21 months whereas 89% (+/+) mice were still alive after 24 months (P < 0.005). There was little mortality in female mice of either genotype. Both (-/-) and (+/+) male mice have normal cardiac dimensions and function at 5.5 months. However, (-/-) mice developed cardiac dilation and dysfunction at 21 months as evidenced by a significant increase (P < 0.05) in left ventricular (LV) end-diastolic diameter from 2.69 +/- 0.13 to 3.13 +/- 0.09 mm, LV end-systolic diameter from 1.28 +/- 0.11 to 1.86 +/- 0.12 mm, LV end-diastolic cavity volume from 21 +/- 2.8 to 31 +/- 2.5 microl and LV mass from 19 +/- 2.5 to 27 +/- 1.9 mg/10 g and a significant decrease (P < 0.05) in ejection fraction (from 65 +/- 3.3% to 41 +/- 4.6%), shortening fraction (from 53 +/- 2.2% to 41 +/- 3.4%), LV posterior wall thickening (from 27 +/- 2% to 12 +/- 4%) and septum thickening (from 27 +/- 2% to 12 +/- 4%) compared with those at 5.5 months. There was a clear increase in cardiac weight and cardiac dilation by hematoxylin and eosin in male (-/-) mice at 21 months. BP in male (-/-) mice fell with the cardiac dysfunction, whereas female (-/-) mice were hypertensive even at 21 months. The level of mRNA for neuronal NOS and inducible NOS was greater in all females compared to males. These results indicate that male (-/-) mice have a significantly shorter lifespan than (+/+) or female mice, and male (-/-) mice develop cardiac dysfunction with age.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
671-80
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15350840-Aging, pubmed-meshheading:15350840-Animals, pubmed-meshheading:15350840-Cardiomegaly, pubmed-meshheading:15350840-Female, pubmed-meshheading:15350840-Gene Expression Regulation, pubmed-meshheading:15350840-Hypertension, pubmed-meshheading:15350840-Longevity, pubmed-meshheading:15350840-Male, pubmed-meshheading:15350840-Mice, pubmed-meshheading:15350840-Mice, Knockout, pubmed-meshheading:15350840-Myocardium, pubmed-meshheading:15350840-Nerve Tissue Proteins, pubmed-meshheading:15350840-Nitric Oxide, pubmed-meshheading:15350840-Nitric Oxide Synthase, pubmed-meshheading:15350840-Nitric Oxide Synthase Type I, pubmed-meshheading:15350840-RNA, Messenger, pubmed-meshheading:15350840-Sex Factors, pubmed-meshheading:15350840-Stroke Volume, pubmed-meshheading:15350840-Ventricular Dysfunction, Left
pubmed:year
2004
pubmed:articleTitle
Premature death and age-related cardiac dysfunction in male eNOS-knockout mice.
pubmed:affiliation
Department of Physiology, New York Medical College, Valhalla, NY, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.