INVESTIGADORES
NOLLY Mariela Beatriz
congresos y reuniones científicas
Título:
Physiologic cardiac hypertrophy: impact of its development upon a model of pathologic hypertrophy.
Autor/es:
ENNIS I.; MARIELA B. NOLLY (PRIMER AUTOR); ANDRÉS OSCAR PINILLA; CAROLINA D. GARCIARENA; PIAGGIO MR; EDUARDO M. ESCUDERO; CINGOLANI HE
Lugar:
Buenos Aires
Reunión:
Congreso; 16th World Congress of Cardiology.; 2008
Resumen:
Physiologic cardiac hypertrophy: impact of its development upon a modelof pathologic hypertrophyI. Ennis1, M.B. Nolly1, O.A. Pinilla1, C.D. Garciarena1, V.B. Carranza1, M.R. Piaggio1, E.M.Escudero1, H.E. Cingolani1. 1Centro de Investigaciones Cardiovasculares. Facultad deCiencias Me´ dicas. UNLP-CONICETPathologic cardiac hypertrophy (CH) is an independent risk factor for cardiovascular morbidityand mortality. It usually leads to heart failure development. On the other hand, cardiachypertrophy induced by intense and periodical execersise training is an adaptive response ofthe myocardium to the increase haemodinamic demand and of course it does not represent arisk factor. The aim of the present work was to analize in spontaneously hypertensive rats (SHR)the effect of intense exercise trainning (swiming, 90 min/day, 5 days a week during 2 months)upon CH and cardiac function. Male SHR (5 month of age) were randomly assigned to a controlgroup (?C?, no physical training) or the excersice group (?E?, swimming rutine). Echocardiographicstudies of each animal were performed at day 1 and day 60 of the protocol. At the endof the protocol the animals were euthanized and hearts kept for histological, biochemical andmolecular analizys. The 60 day swimming rutine induced a significant increase in leftventricular mass determined by ecochardiography (3.020.07 in E vs. 2.760.07 mg/g in C;p0.02), however in the excersised animals a significant reduction in the expression ofmolecular markers of CH was detected by real time RT-PCR: atrial natriuretic peptide (ANP, C:10019; E: 4110 %, p0.05) and myosin light chain-2 (MLC-2, C: 1008; E: 619 %;p0.05). Moreover, exercise training improved cardiac function when measured by themid-ventricular shortening (C: 32.121.01; E: 36.031,34; p0.05). The histological studyrevealed a significant reduction in collagen fraction in the exercised animals. In conclusion, ourresults suggest that intense and programmed exercise training is capable of inducingphysiological CH even in the presence of pathologic CH, leading to an improvement in thehistology, molecular pattern and yet more important in contractility. This finding could beclinically relevant in the prevention of heart failure in patients with pathologic CH.