Source:http://linkedlifedata.com/resource/pubmed/id/15350840
Switch to
Predicate | Object |
---|---|
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 |
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Nos1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
|
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.
|