Challoner D R, Prols H G
J Clin Invest. 1972 Aug;51(8):2071-6. doi: 10.1172/JCI107013.
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.
该实验室先前的研究以及维特尔斯和布雷斯勒所做的研究表明，心肌肉碱耗竭以及随之而来的脂肪酸氧化减少可能与白喉相关的心肌病有关。此外，还发现给予肉碱可延长患白喉豚鼠的存活时间，并改善患白喉犬的心室功能。目前的研究证实了这一假设，即直接测定的心肌肉碱缺陷可在腹腔注射肉碱的患白喉豚鼠中得到补充。先前仅在匀浆中报道的脂肪酸氧化减少在离体灌注的患白喉豚鼠心脏标本中得到了证实。向该灌注液中添加L-肉碱可使脂肪酸氧化增加至正常水平。综合这些研究和先前的研究，将支持肉碱耗竭在白喉性心肌炎发病机制中的作用，并提示用L-肉碱进行实验性治疗的可能性。
