Inhibition of left ventricular remodelling preserves chamber systolic function in pressure-overloaded mice

Alessandro Vergari, G Marano, S Palazzesi, L Catalano, S Gaudi, C Testa, R Canese, G Carpinelli, F Podo, Au Ferrari

Risultato della ricerca: Contributo in rivistaArticolo in rivista

9 Citazioni (Scopus)

Abstract

Controversy exists whether the development of left-ventricular hypertrophy (LVH) is a mechanism able to prevent cardiac dysfunction under conditions of pressure overload. In the present study we re-assessed the long-term effects of attenuating LVH by using L- and D-propranolol, which are equally able to inhibit the development of LVH induced by aortic banding. The aortic arch was banded proximal to the left common carotid artery in 71 CD-1 mice that were then assigned randomly to receive L-propranolol, D-propranolol (both 80 mg/kg per day) or vehicle. Concurrently, sham-operated mice were given L-propranolol, D-propranolol or vehicle. LV dimension and performance were evaluated under isoflurane anaesthesia by cine-magnetic resonance imaging, echocardiography and cardiac catheterization up to 8 weeks after surgery. After 2 weeks of pressure overload, the vehicle-treated banded mice had enhanced LV weight, normal chamber size and increased relative wall thickness (concentric hypertrophy), whereas L-propranolol- or D-propranolol-banded mice showed a markedly blunted hypertrophic response, i.e. normal chamber size and normal relative wall thickness, as well as preserved systolic LV chamber function. After 4 weeks, the vehicle-treated banded mice showed LV enlargement with a reduced relative wall thickness (eccentric remodelling) and a clear-cut deterioration in LV systolic function. In contrast, L-propranolol- or D-propranolol-treated banded mice showed normal chamber size with a normal relative wall thickness and preserved systolic function. A distinct histological feature was that in banded mice, L-or D-propranolol attenuated the development of cardiomyocyte hypertrophy but not the attendant myocardial fibrosis. At the 8-week stage, LV dysfunction was present in propranolol-treated banded mice although it was much less severe than in vehicle-treated banded mice. It is concluded that (i) deterioration of LV systolic performance is delayed if LV hypertrophy is inhibited, (ii) banding-induced deterioration of LV systolic function is associated with LV eccentric remodelling and (iii) the antihypertrophic effect of propranolol is due to a selective action on cardiomyocytes rather than on collagen accumulation
Lingua originaleEnglish
pagine (da-a)429-436
Numero di pagine8
RivistaPFLÜGERS ARCHIV
Volume446
DOI
Stato di pubblicazionePubblicato - 2003

Keywords

  • Animals
  • Aorta
  • Echocardiography
  • Hemodynamics
  • Hypertrophy, Left Ventricular
  • Magnetic Resonance Imaging
  • Male
  • Mice
  • Mice, Inbred Strains
  • Propranolol
  • Systole
  • Vasodilator Agents
  • Ventricular Remodeling

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