Koch M O, McDougal W S
J Urol. 1985 Jul;134(1):162-4. doi: 10.1016/s0022-5347(17)47048-0.
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.
五十多年来，经肠段进行尿路改道后出现的高氯性代谢性酸中毒综合征一直困扰着泌尿外科医生。最近的研究表明，氯丙嗪作为一种肠道环磷酸腺苷抑制剂，可部分纠正与该综合征相关的代谢紊乱。烟酸也已被证明是一种强效的肠道环磷酸腺苷抑制剂。本研究在大鼠膀胱盲肠造口术模型中使用烟酸，以检验其对该综合征的治疗效果。将接受烟酸治疗的膀胱盲肠造口术大鼠与未治疗的大鼠、仅进行肠道改道而非尿路改道的大鼠以及非手术对照组进行比较。每日剂量为50毫克/千克的烟酸可纠正高氯血症（p<0.02）、血清渗透压升高（p<0.0001）、高氨血症（p<0.05）和酸中毒（p<0.001）。结果与在相同模型中使用氯丙嗪所获得的结果相当。
