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Clinical and experimental investigations have shown that the myocardium is highly susceptible to the action of diphtheria toxin (1, 2). Both in man and the guinea pig, one of the earliest altera-tions in the heart muscle exposed to this toxin is fatty degeneration (2, 3). This morphologi-cal observation along with recently acquired evi-dence that fatty acids are a major metabolic sub-strate of the heart (4) suggested that the toxin may exert its effect on the myocardium by inter-fering with fatty acid oxidation. Experiments were designed to test this hypothe-sis by ascertaining the effect of diphtheria toxin on 1) the capacity of the myocardium to oxi-dize long-chain fatty acids, 2) the integrity of component parts of the fatty acid oxidation path-way in the heart, and 3) the concentration of myocardial carnitine (DL-7-trimethylamino-P-hy-droxybutyrate), a compound known to effect a stimulation of long-chain fatty acid oxidation in the heart (5). Methods White, male guinea pigs weighing 250 to 300 g were used. A standard diet consisting of 50 % Purina rabbit chow and 50 % oats supplemented with fresh cabbage was used except as indicated. The experimental ani-mals were divided into 4 groups as follows: a) Diph-theria-toxin 1 animals were injected with toxin sub-cutaneously, the dose being adjusted so that fatty de-generation of the myocardium could be produced regu-larly in surviving animals within 5 days after treatment; b) diphtheria-antitoxin 1 animals were injected intra-peritoneally with 500 U of antitoxin; c) diphtheria-toxin and-antitoxin animals were injected with 500 U of
Wittels et al. (Wed,) studied this question.