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on April 22, 2002

Circulation. 2002
Published online before print April 22, 2002, doi: 10.1161/01.CIR.0000015604.88808.74
A more recent version of this article appeared on May 14, 2002
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Submitted on November 26, 2001
Revised on February 21, 2002
Accepted on February 25, 2002

Cardiac Membrane Fatty Acid Composition Modulates Myocardial Oxygen Consumption and Postischemic Recovery of Contractile Function

Salvatore Pepe PhD and Peter L. McLennan PhD*

From the Cardiac Surgical Research Unit, Alfred Hospital and Baker Medical Research Institute, Monash University Faculty of Medicine (S.P.), Melbourne, Australia; and Smart Foods Centre, Department of Biomedical Science, University of Wollongong (P.L.M.), New South Wales, Australia.

* To whom correspondence should be addressed. E-mail: petermcl{at}uow.edu.au.

Background—Regular fish consumption is associated with low cardiovascular disease morbidity and mortality. Fish oils modify cardiac membrane phospholipid fatty acid composition with potent antiarrhythmic effects. We tested the effects of dietary fish oil on ventricular hemodynamics and myocardial oxygen consumption (MVO2).

Methods and Results—Male Wistar rats were fed for 16 weeks on a reference diet rich in n-6 polyunsaturated fatty acids (PUFA), a diet rich in saturated animal fat (SAT), or a diet rich in n-3 PUFA from fish oil. Isolated working hearts were perfused with porcine erythrocytes (40% hematocrit) at 75 mm Hg afterload with variable preload (5 to 20 mm Hg) or with low coronary flow ischemia with maintained afterload, preload, and heart rate, then reperfused. MVO2 was low and coronary perfusion reserve high in n-3 PUFA hearts, and cardiac output increased with workload. The n-3 PUFA reduced ischemic markers—acidosis, K+, lactate, and creatine kinase—and increased contractile recovery during reperfusion. SAT hearts had high MVO2, low coronary perfusion reserve, and poor contractile function and recovery. Dietary differences in MVO2 were abolished by KCl arrest (basal metabolism) or ruthenium red (3.4 µmol/L) but not by ryanodine (1 nmol/L). Fish oil or ryanodine, but not ruthenium red, prevented ventricular fibrillation in reperfusion.

Conclusions—Dietary fish oil directly influenced heart function and improved cardiac responses to ischemia and reperfusion. The n-3 PUFA reduced oxygen consumption at any given work output and increased postischemic recovery. Thus, direct effects on myocardial function may contribute to the altered cardiovascular disease profile associated with fish consumption.


Key words: myocardium • oxygen • ischemia • fatty acids • fish oils




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