Gottrup F, Ornsholt J
Scand J Gastroenterol. 1978;13(3):337-43. doi: 10.3109/00365527809179830.
The effect of salmefamol, a new beta 2-agonist, on pentagastrin-induced gastric acid secretion was studied in conscious gastric fistula dogs. Salmefamol inhibited the acid secretion, an effect which was dose dependent. The volume as well as the acidity was inhibited. Salmefamol caused an increase in the pulse rate. Propranolol prevented the inhibition of acid output as well as the increase in pulse rate. Practolol, a beta 1-adrenoceptor blocker, had no effect on the inhibition of acid secretion but prevented the increase in pulse rate. Dose-response experiments with 6 doses of pentagastrin and 1 dose of salmefamol showed a decrease in calculated maximal response (CMR) and an unchanged D50. It is concluded that salmefamol strongly inhibits pentagastrin-induced acid output in the dog, and the inhibition follows a non-competitive kinetic. The mechanism of gastric secretion probably involves a beta 2-receptor.
在清醒胃瘘犬中研究了新型β2激动剂沙美特罗对五肽胃泌素诱导的胃酸分泌的影响。沙美特罗抑制胃酸分泌，该作用呈剂量依赖性。分泌量和酸度均受到抑制。沙美特罗导致心率增加。普萘洛尔可防止胃酸分泌抑制以及心率增加。醋丁洛尔，一种β1肾上腺素受体阻滞剂，对胃酸分泌抑制无作用，但可防止心率增加。用6种剂量的五肽胃泌素和1种剂量的沙美特罗进行的剂量反应实验显示计算的最大反应（CMR）降低而D50不变。得出结论，沙美特罗强烈抑制犬五肽胃泌素诱导的胃酸分泌，且该抑制遵循非竞争性动力学。胃酸分泌机制可能涉及β2受体。
