Nicotinic acid: treatment for the hyperchloremic acidosis following urinary diversion through intestinal segments.
The syndrome of hyperchloremic metabolic acidosis following urinary diversion through intestinal segments has posed a problem for urologists for more than 50 years. Recent work demonstrates that chlorpromazine, an intestinal cyclic-AMP inhibitor, partially corrects the metabolic derangements associated with this syndrome. Nicotinic acid has also been shown to be a potent inhibitor of intestinal cyclic-AMP. The present investigation employs nicotinic acid in a rat vesico-cecostomy model to examine its efficacy in the management of this syndrome. Rats with vesico-cecostomies treated with nicotinic acid are compared to untreated rats, rats with intestinal but not urinary diversions and non-operative controls. Nicotinic acid in a dose of 50 mg./kg./day corrects the hyperchloremia (p less than 0.02), elevated serum osmolality (p less than 0.0001), hyperammoniumemia (p less than 0.05) and acidosis (p less than 0.001). Results compare favorably to those obtained in an identical model with the use of chlorpromazine.
D000138:Acidosis / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D000818:Animals; D002432:Cecum / Q000601:surgery; D002712:Chlorides / Q000378:metabolism*; D002746:Chlorpromazine / Q000627:therapeutic use; D003106:Colon / Q000601:surgery; D008297:Male; D009525:Niacin / Q000627:therapeutic use*; D009994:Osmolar Concentration; D051381:Rats; D014547:Urinary Diversion / Q000009:adverse effects*
D002712:Chlorides; D009525:Niacin; D002746:Chlorpromazine