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

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Abstract
The hemodynamic and metabolic effects of treatments with the L and DL-isomers of carnitine in 4 groups (n = 42) of intact working swine hearts rendered mildly ischemic (-46% reduction in global perfusion) were studied. In 3 groups (n = 34), free fatty acids (FFA) in the coronary perfusate were augmented with labeled palmitate (0.72 .mu.mol/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 14CO2 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 O2 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 and 14CO2 production were signifiantly 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. Carnitine apparently reduces availability or incorporation of FFA intracellularly. This benefits the heart mechanically during ischemic restrictions in coronary flow. The L-isomer appears to be more biologically active.

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