Liver mitochondria, confirmed as intact by complete suppression of succinate uptake and oxidation, possess a carnitine palmitoyltransferase I that is totally inhibited by malonyl CoA.

Succinate dehydrogenase activity in mitochondria, which were isolated by centrifuging partially purified mitochondria through 1. 315 M sucrose, was completely suppressed when [14C]succinate uptake was abolished by prior incubation of the mitochondria with carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) and valinomycin. The conclusion that these mitochondria were intact was confirmed by the fact that, when these mitochondria were broken by a freeze-thaw cycle followed by sonication, such inhibition was totally abolished. The yield of mitochondria, microsomes, and peroxisomes from the initial homogenate was 17.8, <0.1, and 0%, respectively, indicating that the mitochondria were not only intact but also essentially free of contamination from microsomes and peroxisomes. The overt form of carnitine palmitoyltransferase (CPT I) in these intact and pure mitochondria was totally inhibited by malonyl CoA, indicating that previous reports of incomplete inhibition in mitochondrial preparations resulted from interference from CPT activity in the inner mitochondrial membrane (CPT II), microsomes, or peroxisomes.     

Causalgia pathogenesis and treatment

Gross and microscopic anatomical evidence indicates that pain fibers involved in causalgia are those distributed to blood vessels-possibly to the arterioles-and that, for the greater part, these fibers constitute part of the general visceral afferent system. Several investigators have reported evidence that injury to a peripheral nerve of such a type as to cause damage to the vasomotor control of any area produces the initial pain in an extremity, and it is predicated that the arteriolar constriction causing the pain is then prolonged by the sensitization of arteriolar smooth muscle to the amount of epinephrine normally in the blood. If the condition is not treated, tissue anoxia occurs to such an extent that irreversible changes take place in the affected area.Treatment of causalgia in the lower extremities is directed toward interruption of either the vasomotor or afferent supply of blood vessels by blocking or excision of the second to fourth lumbar ganglia inclusive with the intervening chains. For the upper extremities, the blocking or disconnection of the second and third thoracic ganglia with interruption of the sympathetic chain between the third and fourth ganglia is considered a feasible method of treatment which does not produce the concomitant disability of Horner's syndrome.