Long-chain acylcarnitines accumulate during
myocardial ischemia and contribute to membrane dysfunction in ischemic zones. On the basis of the 3-fold selectivity for
saturated fatty acid accumulation during
myocardial ischemia, it was implicitly assumed that saturated long chain
acylcarnitine molecular species predominantly accumulated in ischemic myocardium. By exploiting the analytical power of electrospray ionization mass spectroscopy, we now report that unsaturated acylcarnitines are the predominant molecular species of
acylcarnitine which accumulate during
myocardial ischemia (rank order: octadecadienoyl
carnitine > octadecanoyl
carnitine > hexadecanoyl
carnitine > octadecanoyl
carnitine). The aliphatic chain distribution of myocardial
acylcarnitine molecular species identified by electrospray ionization mass spectroscopy was independently substantiated by sequential HPLC purification and capillary gas chromatography. Detailed analysis of the individual molecular species of long-chain
acylcarnitine demonstrated that fatty acyl chain elongation was prominent in ischemic myocardium (e.g., following 20 min of
ischemia, greater than 15% of the accumulated acylcarnitines consisted of 20-
carbon unsaturated molecular species). Chain-elongated
lipids were essentially confined to the long chain
acylcarnitine pool since [9,10-3H]octadec-9'-enoic
acid was converted to [3H]eicosenoyl
carnitine (12% of the radiolabeled
acylcarnitine pool) in ischemic hearts without substantive amounts of [3H]eicosenoyl residues in the
fatty acid,
triglyceride, and
phospholipid pools. Collectively, these results demonstrate the preponderance of unsaturated acylcarnitines in ischemic myocardium and document the metabolic compartmentation of downstream products of fatty acyl chain elongation in the
acylcarnitine pool during
ischemia.