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F4. Myocardial Protection Using An Omega-3 Fatty Acid Infusion: Quantification And Mechanism Of Action.
Jonathan Mcguinness, David Bouchier-hayes, J. Mark Redmond; Dublin, Ireland

Objective: Omega-3 fatty acids confer a cardiac survival advantage with prolonged oral supplementation. We sought to delineate the extent of myocardial protection and mechanism of action with acute intravenous supplementation.
Methods: Male New-Zealand white rabbits recieved an intravenous infusion of either an omega-3 fatty acid emulsion used in TPN for 4 days pre-operatively and prior to surgery, or an equivalent infusion of 0.9% saline (n=14 in each group). Subsequently, the large marginal branch of the left coronary artery was occluded for 30mins, functional assessment performed during the 3hours of reperfusion, and measurment of infarct size. Pretreatment-induced alterations in myocardial membrane fatty acid composition, along with intra-myocardial heat shock protein 72 and serum nitrite levels(markers of delayed preconditioning) were evaluated. Markers of fatty acid free radical injury were studied during the 3 hours of reperfusion.
Results: Pretreatment resulted in an increase in the myocardial membrane omega 3 fatty acid content(5.38%+/-0.44 vs 0.947%+/-0.07 control,P<0.0001), a 225% elevation of heat shock protein 72 levels(P=0.019), and lower serum nitrite levels(153+/-19 vs 234+/-22 micromolar in controls P=0.037) prior to ischaemia-reperfusion. This was associated with a 40% reduction in infarct size(Figure,P<0.0001). Pretreatment produced higher malonaldehyde levels(10.2+/-1.5 vs 6.1+/-0.7 micromolar in controls P=0.04), a relatively inert product of polyunsaturated fatty acid peroxidation, and a 9 fold reduction in 8-Isoprostanes(74+/-45 vs 679+/-190 pg/ml in controls P=0.0077), the toxic byproduct of arachidonic acid oxidant injury.
Conclusions: The reduction in 8-Isoprostane levels in the pretreated group and corresponding increase in malonaldehyde levels suggest a shift in the oxidant ischaemia-reperfusion injury away from arachidonic acid which is structurally and functionally important to the myocardial membrane, and instead diverted towards the additional Omega-3 fatty acids in the pretreated myocardial membrane. Additionally, the enhanced heat shock protein 72 levels in the pretreated heart suggest preconditioning-type protection. The significant myocardial preservation afforded by an intravenous Omega-3 fatty acid infusion warrants further investigation in the modern era in which patients with more borderline left ventricular function are being referred for more complex, lengthy procedures.

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