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Dietary fish oil preserves cardiac function in the hypertrophied rat heart

McLennan, Peter L. ; Abeywardena, Mahinda Y. ; Dallimore, Julie A. ; Raederstorff, Daniel

In: British Journal of Nutrition, 2012, vol. 108, no. 4, p. 645-654

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    Titre
    • Dietary fish oil preserves cardiac function in the hypertrophied rat heart
    Auteur
    • McLennan, Peter L.. Cardiovascular Research Laboratory, Graduate School of Medicine, University of Wollongong, Wollongong, NSW 2522, Australia
    • Abeywardena, Mahinda Y.. CSIRO Human Nutrition, Adelaide, Australia
    • Dallimore, Julie A.. CSIRO Human Nutrition, Adelaide, Australia
    • Raederstorff, Daniel. DSM Nutritional Products, Basel, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • British Journal of Nutrition, 2012, vol. 108, no. 4, p. 645-654. Cambridge University Press
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:294756
    Summary
    Regular fish or fish oil intake is associated with a low incidence of heart failure clinically, and fish oil-induced reduction in cardiac remodelling seen in hypertrophy models may contribute. We investigated whether improved cardiac energy efficiency in non-hypertrophied hearts translates into attenuation of cardiac dysfunction in hypertrophied hearts. Male Wistar rats (n 33) at 8 weeks of age were sham-operated or subjected to abdominal aortic stenosis to produce pressure-overload cardiac hypertrophy. Starting 3 weeks post-operatively to follow initiation of hypertrophy, rats were fed a diet containing 10% olive oil (control) or 5% fish oil (ROPUFA® 30 (17% EPA, 10% DHA))+5% olive oil (FO diet). At 15 weeks post-operatively, ventricular haemodynamics and oxygen consumption were evaluated in the blood-perfused, isolated working heart. Resting and maximally stimulated cardiac output and external work were >60% depressed in hypertrophied control hearts but this was prevented by FO feeding, without attenuating hypertrophy. Cardiac energy efficiency was lower in hypertrophy, but greater in FO hearts for any given cardiac mass. Coronary blood flow, restricted in hypertrophied control hearts, increased with increasing work in hypertrophied FO hearts, revealing a significant coronary vasodilator reserve. Pronounced cardiac dysfunction in hypertrophied hearts across low and high workloads, indicative of heart failure, was attenuated by FO feeding in association with membrane incorporation of n-3 PUFA, principally DHA. Dietary fish oil may offer a new approach to balancing the high oxygen demand and haemodynamic requirements of the failing hypertrophied heart independently of attenuating hypertrophy