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We studied the hemodynamic and metabolic effects of treatments with the L- and DL- isomers of carnitine in four groups (n = 42) of intact working swine hearts rendered mildly ischemic (−46% reduction in global perfusion). In three groups (n = 34), free fatty acids (FFA) in the coronary perfusate were augmented with labeled palmitate (0.72 /μnol/ml). The inclusion of excess FFA per se (n = 11), as compared with nonsupplemented hearts, further and significantly depressed mechanical function (−40% and −55% declines in left ventricular (LV)-developed pressure and work), stimulated a 2-fold increase in FFA uptake (but without a corresponding increase in “CO2 production), raised fatty acyl-CoA levels in tissue (94 to 132 nmol/g dry), and shortened group survival. Treatments with both L- and DL-carnitine (serum values 6687 and 6398 nmol/ml) effected significant improvements in several parameters of mechanical function and survival. LV-developed pressure and work at end-ischemia were increased (+50% and +62% in L-treated hearts and +48% and +65% in DL-treated hearts). Myocardial oxygen consumption was similar to that of untreated FFA-supplemented hearts. During the middle to late portion of the perfusion trials in L-treated hearts (n = 9), FFA uptake and14CO2production were significantly reduced, and accumulation of tissue long-chain acyl-CoA was less (−44%, P < 0.05). Metabolic trends in DL-carnitine-treated hearts ranged between those in untreated and L- carnitine-treated hearts. These data suggest that carnitine reduces availability or incorporation of FFA intracellularly, and this benefits the heart mechanically during ischemic restrictions in coronary flow. The L-isomer appears to be the more biologically active.

Effects of carnitine isomers on fatty acid metabolism in ischemic swine hearts.