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Addition of halothane to the incubation medium is shown to lower respiratory control and transmembrane potential and to increase ATPase activity in isolated rat liver mitochondria. Evidence is presented that L-carnitine is able to substantially decrease the negative effects of halothane on the energy-linked processes of mitochondria. The effects of halothane and the protective action of L-carnitine are discussed in the light of a possible involvement of long-chain acyl CoA in the unpairing of mitochondrial energy-linked functions.

Incubation of rat liver mitochondria in the presence of halothane induced a consistent impairment of mitochondrial oxidative phosphorylation without significantly affecting the steady-state of transmembrane electrical potential. These alterations of mitochondrial energy-linked processes were associated with a consistent accumulation of long-chain acyl CoA. Addition of L-carnitine partially prevented the effects of halothane on oxidative phosphorylation and completely abolished the halothane-induced long-chain acyl CoA accumulation. The possibility is discussed that the damaging action of halothane on mitochondrial functions might be partially ascribed to the noxious action of the excess of long-chain acyl CoA induced the anesthetic.

Myocardial triglyceride levels in rats fed a high erucic acid rapeseed oil diet for three days were five times higher than in controls. The incorporation of erucic acid and, to a lower extent, some unsaturated fatty acids was increased, as well as total cholesterol content, compared to controls. The presence of 5% carnitine in the diet partially prevented these effects. It is assumed that carnitine may be a rate limiting factor in the myocardial catabolism of unsaturated fatty acids and particularly erucic acid, when these substance are ingested in supraoptimal amount.