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 < 0.02), elevated serum osmolality (p < 0.0001), hyperammoniumemia (p < 0.05) and acidosis (p < 0.001). Results compare favorably to those obtained in an identical model with the use of chlorpromazine.
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