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Cardiac hypertrophy, animal models

Cardiovascular Disease. Animal studies show that severe copper deficiency causes cardiac damage, but the abnormality differs from that seen in human cardiovascular disease. The myocardium is hypertrophied and may rupture in animal models. Coronary artery pressure is decreased, but in human ischemic disease it is increased. The role of copper in human cardiovascular disease is controversial, although much supporting evidence for a positive link with low dietary copper intake has been published. ... [Pg.1129]

Research in both animal models and in clinical practice has shown that circulating BNP is a marker of myocyte hypertrophy and useful in the clinical management of acute and chronic heart failure [21, 94, 95]. BNP is specifically expressed by cardiac myocytes during cardiogenesis and is induced and released under conditions which can lead to cardiac hypertrophy including mechanical stress, ischemia, inflammation, and drug-induced toxicity [86], Pro-BNP is cleaved into NT-pro-BNP and BNP, and NT-pro-BNP... [Pg.469]

There are several models of cardiac hypertrophy, heart disease and heart failure in small animals, particularly the rat. Proteomic analysis of these models has focussed on changes in cardiac proteins in response to alcohol (Patel et al., 1997 Patel et al., 2000) and lead (Toraason et al., 1997) toxicity. Unfortunately the cardiac physiology of small animal models and their normal pattern of gene expression (e.g. isoforms of the major cardiac contractile proteins) differ from that in larger mammals such as humans. Therefore investigations have moved into higher mammals and recently two... [Pg.41]


See other pages where Cardiac hypertrophy, animal models is mentioned: [Pg.389]    [Pg.129]    [Pg.8]    [Pg.34]    [Pg.232]    [Pg.252]    [Pg.301]    [Pg.325]    [Pg.329]    [Pg.419]    [Pg.269]    [Pg.270]    [Pg.387]    [Pg.537]    [Pg.306]   
See also in sourсe #XX -- [ Pg.301 ]




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Animal models

Cardiac hypertrophy

Cardiac modeling

Hypertrophy

Model animal models

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