Chlorpromazine: adjuvant therapy for the metabolic derangements created by urinary diversion through intestinal segments.
The hyperchloremic metabolic acidosis which can occur following urinary diversion through intestinal segments has been managed with bicarbonate or citrate salts. However, satisfactory management is not always possible with this form of treatment. The development of this acidosis has been attributed to intestinal reabsorption of urinary solutes or intestinal secretion of bicarbonate. Intestinal absorptive and secretory processes are modulated by an adenylate cyclase-cyclic AMP system. Chlorpromazine inhibits the effect of cyclic AMP on the intestinal mucosal cell. The use of chlorpromazine in the management of the hyperchloremic metabolic acidosis following urinary diversion was investigated. A canine model employing an ileal segment between ureter and bladder and a rat model in which urine is diverted through the entire colon have been developed. Chlorpromazine (5 mg./kg./day) was found to be efficacious in the management of the metabolic derangements that occur in both of these models. A case study is presented in which conventional management of this syndrome with bicarbonate salts was unsuccessful. The use of chlorpromazine as an adjuvant treatment allowed correction of the acidosis.[1]References
- Chlorpromazine: adjuvant therapy for the metabolic derangements created by urinary diversion through intestinal segments. Koch, M.O., McDougal, W.S. J. Urol. (1985) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
