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Titolo:
Modulation of in vivo cardiac hypertrophy with insulin-like growth factor-1 and angiotensin-converting enzyme inhibitor: Relationship between change in myosin isoform and progression of left ventricular dysfunction
Autore:
Iwanaga, Y; Kihara, Y; Yoneda, T; Aoyama, T; Sasayama, S;
Indirizzi:
Kyoto Univ, Grad Sch Med, Dept Cardiovasc Med, Sakyo Ku, Kyoto 6068507, Japan Kyoto Univ Kyoto Japan 6068507 ovasc Med, Sakyo Ku, Kyoto 6068507, Japan
Titolo Testata:
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
fascicolo: 2, volume: 36, anno: 2000,
pagine: 635 -
SICI:
0735-1097(200008)36:2<635:MOIVCH>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHRONIC HEART-FAILURE; FACTOR-I; DILATED CARDIOMYOPATHY; HEAVY-CHAIN; HYPERTENSIVE RATS; GENE-EXPRESSION; ATPASE ACTIVITY; ALPHA-MYOSIN; SHORT-TERM; HORMONE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Kihara, Y Kyoto Univ, Grad Sch Med, Dept Cardiovasc Med, Sakyo Ku, 54 Shogoin Kawaharacho, Kyoto 6068507, Japan Kyoto Univ 54 Shogoin Kawaharacho Kyoto Japan 6068507 07, Japan
Citazione:
Y. Iwanaga et al., "Modulation of in vivo cardiac hypertrophy with insulin-like growth factor-1 and angiotensin-converting enzyme inhibitor: Relationship between change in myosin isoform and progression of left ventricular dysfunction", J AM COL C, 36(2), 2000, pp. 635

Abstract

OBJECTIVES Supplemental myocardial hypertrophy induced by insulin-like growth factor (IGF)-1 may prevent transition from hypertrophy to heart failureunder chronic mechanical overload. BACKGROUND Several studies have suggested that IGF-1 treatment may be beneficial in chronic heart failure. In addition, recent studies indicated thatthe amount of cu-myosin heavy chain (MHC) plays a significant hemodynamic role in large animals including humans. METHODS We treated Dahl salt-sensitive hypertensive rats on a long-term basis with IGF-1. The effects were compared with those produced by treatment using a sub-antihypertensive dose of temocapril, an angiotensin-converting enzyme (ACE) inhibitor. At 11 weeks, when these rats displayed compensated left ventricular hypertrophy (LVH), they were randomized to three groups: 1) TGF group (3 mg/kg/day); 2) temocapril group (1 mg/kg/day); and 3) vehicle (control) group. RESULTS After 15 weeks, the control rats showed left ventricular (LV) enlargement and severe LV dysfunction and rapidly died of pulmonary congestion (mean survival time: 16.8 +/- 0.5 weeks). The survival time was significantly shortened (15.6 +/- 0.3 weeks) in the IGF-1 group but significantly prolonged (19.5 +/- 0.6 weeks) in the temocapril group. The rats in the IGF-1 group showed accelerated LV dilation and dysfunction. Of the several parameters investigated, it was found that the relative amounts of MHC isoforms differed among the three groups. The alpha-MHC mRNA level was decreased by 52% (p < 0.01) in the IGF group, while it increased by 58% (p < 0.01) in the temocapril group compared with the control group. These changes were related to the progression of LV dysfunction. CONCLUSIONS Supplemental myocardial hypertrophy with long-term IGF-1 treatment may not be beneficial if concentric LVH already exists. Our data suggest that IGF-1 may not protect myocardial performance when its hypertrophic effect aggravates the reduction of alpha-MHC. By contrast, the ACE inhibitor may improve myocardial function and prognosis by preventing the down-regulation of this isoform. (C) 2000 by the American College of Cardiology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 23:41:30