Previous studies from this laboratory and by Wittels and Bressler have suggested that myocardial carnitine depletion and an accompanying decrease in fatty acid oxidation may contribute to the myocardial disease associated with diphtheria. In addition, administration of carnitine was found to prolong survival of diphtheritic guinea pigs and improve ventricular function in diphtheritic dogs. The present studies document the hypothesis that the defect in myocardial carnitine, directly assayed, could be repleted in diphtheritic guinea pigs to whom carnitine was administered intraperitoneally. The decreased fatty acid oxidation previously reported only for homogenates was confirmed in an isolated perfused diphtheritic guinea pig heart preparation. The addition of L-carnitine to this perfusate augmented fatty acid oxidation to normal levels. Taken together, these and previous studies would support a pathogenetic role for carnitine depletion in diphtheritic myocarditis and suggest the possibility of experimental therapy with L-carnitine.
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Challoner et al. (1972) studied this question.
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