Chlorpromazine enzyme inhibition

Pharmacokinetic. Agents metabolised in the liver provide higher plasma concentrations when another drug that inhibits hepatic metabolism, e.g. cimetidine, is added. Enzyme inducers enhance the metabolism of this class of P-blockers. P-adrenoceptor blockers themselves reduce hepatic blood flow (fall in cardiac output) and reduce the metabolism of p-blockers and other drugs whose metabolic elimination is dependent on the rate of delivery to the liver, e.g. lignocaine (lidocaine), chlorpromazine. 

Carbamazepine induces hepatic microsomal enzymes that can decrease the steady-state plasma levels of phenothiazines (reported mainly with chlorpromazine, fluphenazine, and perphenazine). Chlorpromazine and thioridazine may increase the serum levels of phenytoin due to its inhibition of hepatic mono-oxygenase activities. 

After 2 to 3 weeks of chronic treatment, a 40% decline in AUC was observed as a result of inhibition of its own absorption due to decreased GI motility, or because chlorpromazine may accelerate its own metabolism through enzyme induction. 

Anti-inflammatory corticosteroids reduce PG production in vivo but not in vitro. They induce the synthesis and/or release of two proteins macrocortin , MW 15,000, first isolated from perfused guinea pig lungs, and lipomodulin , MW 40,000, isolated from rabbit neutrophils. These have been reported to inhibit phospholipase A2 (Blackwell and Flower 1983), but definite proof is still lacking (Bonney and Humes 1984). It is not known whether similar proteins are induced within the CNS. Mepacrine, chlorpromazine, and halothane are all reported to inhibit the enzyme (Blackwell and Flower 1983). 

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