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倍他唑诱导的胃抑肽分泌并非由胃盐酸介导。

Betazole-induced GIP secretion is not mediated by gastric HCl.

作者信息

Spitz I M, Novis B H, Ebert R, Trestian S, LeRoith D, Creutzfeldt W

出版信息

Metabolism. 1982 Apr;31(4):380-2. doi: 10.1016/0026-0495(82)90114-7.

Abstract

Betazole, a pyrazole analogue of histamine, as well as pentagastrin and HCl stimulate GIP secretion. We have asked the question as to whether betazole acts directly or via the production of HCl. Eight normal subjects and 4 patients with achlorhydria secondary to pernicious anemia were given betazole (0.5 mg/kg) by IM injection. Another six normal subjects were also given betazole but this was preceded by 200 mgs. of the H2 receptor blocker cimetidine given IV 60 mins. previously and a slow infusion of 200 mg. cimetidine given over the next 4 hr. Our results have shown that the GIP response to betazole is maintained in achlorhydric subjects as well as during H2 blockade. The results suggest that betazole and therefore histamine may stimulate GIP directly and not necessarily via the mediation of HCl.

摘要

倍他唑是组胺的吡唑类似物,与五肽胃泌素和盐酸一样,能刺激胃肠抑胃肽(GIP)的分泌。我们提出了一个问题,即倍他唑是直接起作用还是通过盐酸的产生来发挥作用。对8名正常受试者和4名因恶性贫血继发胃酸缺乏的患者进行了肌肉注射倍他唑(0.5毫克/千克)的操作。另外6名正常受试者也接受了倍他唑,但在此之前60分钟静脉注射了200毫克H2受体阻滞剂西咪替丁,并在接下来的4小时内缓慢输注200毫克西咪替丁。我们的结果表明,在胃酸缺乏的受试者以及H2受体阻断期间,对倍他唑的GIP反应得以维持。结果提示,倍他唑以及组胺可能直接刺激GIP,而不一定通过盐酸的介导。

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