Cardiovascular Research Advance Access [Accepted Manuscript] published online on December 18, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm109
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EXERCISE PROMOTES ANGIOGENESIS AND IMPROVES β-ADRENERGIC RECEPTOR SIGNALING IN THE POST-ISCHEMIC FAILING RAT HEART
a Dipartimento di Medicina Clinica, Scienze Cardiovascolari ed Immunologiche, Università Federico II, Napoli, Italy
b Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA, USA
c Fondazione S. Maugeri – IRCCS, Telese, Italy
d Dipartimento di Scienze Biomorfologiche e Funzionali, Università Federico II, Napoli, Italy
e Dipartimento di Medicina Sperimentale e Centro di Eccellenza delle Malattie Cardiovascolari, 2
Università di Napoli, Italy
f Dipartimento di Scienze della Salute, Università del Molise, Italy
Correspondence to Dario Leosco, MD, PhD, Cattedra di Geriatria, Università Federico II, Via Pansini 5, 80131 Naples, Italy. e-mail: dleosco{at}unina.it; tel. +39.081.7462267; fax. +39.081.7462339.
Aims: We investigated whether exercise training could promote angiogenesis and improve blood perfusion and left ventricular remodelling of the post-myocardial infarction failing heart. We also explored the contribution of ameliorated β-adrenergic receptor signaling and function on the overall improvement of cardiac contractility reserve induced by exercise.
Methods: Adult Wistar male rats were randomly assigned to one of four experimental groups. Sham-operated and post-myocardial infarction heart failure rats were housed under sedentary conditions or assigned to 10-weeks of a treadmill exercise protocol.
Results: At 4 weeks after myocardial infarction, sedentary heart failure rats showed left ventricular eccentric hypertrophy, marked increase of left ventricular diameters associated with severely impaired fractional shortening (14 ± 5%), increased left ventricular end diastolic pressure (20.9 ± 2.6 mmHg), and pulmonary congestion. In addition, cardiac contractile responses to adrenergic stimulation were significantly blunted. In trained heart failure rats, exercise was able to (1) reactivate the cardiac vascular endothelial growth factor pathway with a concurrent enhancement of myocardial angiogenesis, (2) significantly increase myocardial perfusion and coronary reserve, (3) reduce cardiac diameters, and (4) improve left ventricular contractility in response to adrenergic stimulation. This latter finding was also associated with a significant improvement of cardiac β-adrenergic receptor downregulation and desensitization.
Conclusions: Our data indicate that exercise favourably affects angiogenesis and improves left ventricular remodelling and contractility reserve in a rat model of severe chronic heart failure.
Time for primary review: 27
Dario Leosco and Giuseppe Rengo were co-first authors of this work
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