在雄性大鼠中，苯丙胺通过一种涉及胆囊收缩素分泌增加的机制抑制胃排空和肠道转运。

Inhibition of gastric emptying and intestinal transit by amphetamine through a mechanism involving an increased secretion of CCK in male rats.

Doong M L, Lu C C, Kau M M, Tsai S C, Chiao Y C, Chen J J, Yeh J Y, Lin H, Huang S W, Chen T S, Chang F Y, Wang P S

Department and Graduate Institute of Physiology, National Yang-Ming University, Taipei, Taiwan, Republic of China.

Br J Pharmacol. 1998 Jul;124(6):1123-30. doi: 10.1038/sj.bjp.0701937.

Abstract

The effect of amphetamine on gastrointestinal (GI) transit and the plasma levels of cholecystokinin (CCK) were studied in male rats. 2. Gastric emptying was inhibited both acutely and chronically by the administration of amphetamine. GI transit was decreased by the acute administration of amphetamine but not affected by the chronic administration of amphetamine. 3. Plasma CCK levels were increased dose-dependently by amphetamine. 4. Proglumide, a CCK receptor antagonist, prevented amphetamine-induced inhibition of gastric emptying and the decrease in GI transit in male rats. 5. The selective CCK(A) receptor antagonist, lorglumide, dose-dependently attenuated the amphetamine-induced inhibition of gastric emptying in male rats. In contrast, the selective CCK(B) receptor antagonist, PD 135,158, did not reverse the effect of amphetamine on gastric emptying. 6. Both lorglumide and PD 135,158 reversed the inhibitory effect of amphetamine on GI transit in male rats. 7. These results suggest that amphetamine-induced inhibition of gastric emptying and intestinal transit is due in part to a mechanism associated with the hypersecretion of endogenous CCK.

摘要

在雄性大鼠中研究了苯丙胺对胃肠（GI）转运及胆囊收缩素（CCK）血浆水平的影响。2. 苯丙胺的急性和慢性给药均抑制胃排空。苯丙胺急性给药可使GI转运降低，但慢性给药对其无影响。3. 苯丙胺使血浆CCK水平呈剂量依赖性升高。4. 一种CCK受体拮抗剂丙谷胺可防止苯丙胺诱导的雄性大鼠胃排空抑制及GI转运降低。5. 选择性CCK（A）受体拮抗剂洛谷胺可剂量依赖性减弱苯丙胺诱导的雄性大鼠胃排空抑制。相反，选择性CCK（B）受体拮抗剂PD 135,158不能逆转苯丙胺对胃排空的作用。6. 洛谷胺和PD 135,158均可逆转苯丙胺对雄性大鼠GI转运的抑制作用。7. 这些结果表明，苯丙胺诱导的胃排空和肠道转运抑制部分归因于与内源性CCK分泌过多相关的机制。