a1 TIMC-IMAG, CNRS UMR 5525, Laboratoire PRETA Cœur et Nutrition, Faculté de Médecine, Université Joseph Fourier, Grenoble, France
a2 Laboratoire de Bioénergétique INSERM E221, Université Joseph Fourier, Grenoble, France
Moderate ethanol drinking (ED) and n-3 fatty acids have both been associated with low cardiac mortality. However, there are few data evaluating the interactions of ED with n-3. We recently reported that moderate ED results in increased n-3 in cardiac patients. The main aim of the present study was, through a well-controlled experimental model, to confirm that chronic ED actually results in increased n-3. Secondary aims were to examine the effects of chronic ED on cardiac mitochondria, cardiac function and experimental myocardial infarction. We studied the fatty acid profiles of plasma, cell membranes and cardiac mitochondria phospholipids in a rat model of chronic ED. In plasma and cell membranes, ED actually resulted in higher n-3 (P = 0·005). In mitochondria phospholipids of ED rats, n-3 were also increased (P < 0·05) but quite modestly. Cardiac mitochondrial function and left ventricular function were not significantly different in ED and control rats, while infarct size after 30 min ischaemia and reperfusion was smaller (P < 0·0001) in ED rats. This is the first animal study confirming interaction of alcohol drinking with n-3. We found no harmful effect of chronic ED on the heart in that model but a significant cardioprotection. Further studies are warranted to investigate the mechanisms by which moderate ED alters the metabolism of n-3 and whether n-3 are the mediators of the ED-induced cardioprotection.
(Received November 30 2007)
(Revised February 18 2008)
(Accepted March 14 2008)
(Online publication April 29 2008)
Abbreviations: ED, ethanol drinking; LV, left ventricular