Holst J J, Grønholt R, Schaffalitzky de Muckadell O B, Fahrenkrug J
Acta Physiol Scand. 1981;113(3):273-8. doi: 10.1111/j.1748-1716.1981.tb06896.x.
We studied the effect of a primed i.v. infusion of somatostatin (0.5 microgram x min-1 x kg-1) on the glucose dependent insulin and glucagon responses to electrical stimulation of the vagus nerves or to i.a. acetylcholine in anesthetized pigs. Somatostatin completely abolished the insulin and glucagon responses to ongoing vagal stimulation; after 70 min somatostatin infusion the response to reiterated stimulation was profoundly inhibited. After termination of the somatostatin infusion, a considerable rebound secretion of insulin and glucagon was noted. By contrast, the endocrine response to acetylcholine persisted in spite of the somatostatin administration. Blood glucose increased slightly during somatostatin infusion. The results suggest that somatostatin inhibits the responses to vagal stimulation by interference with the neural transmission to the pancreatic islets rather than by inhibition of the islet cells themselves; acetylcholine may be involved in this neural transmission (acting on nicotinic receptors).
我们研究了静脉给予负荷剂量的生长抑素（0.5微克·分钟⁻¹·千克⁻¹）对麻醉猪在迷走神经电刺激或腹腔注射乙酰胆碱后，葡萄糖依赖性胰岛素和胰高血糖素反应的影响。生长抑素完全消除了对持续迷走神经刺激的胰岛素和胰高血糖素反应；在输注生长抑素70分钟后，对重复刺激的反应受到显著抑制。在生长抑素输注终止后，观察到胰岛素和胰高血糖素出现相当程度的分泌反弹。相比之下，尽管给予了生长抑素，对乙酰胆碱的内分泌反应仍然存在。在生长抑素输注期间，血糖略有升高。结果表明，生长抑素通过干扰向胰岛的神经传递而非抑制胰岛细胞本身来抑制对迷走神经刺激的反应；乙酰胆碱可能参与了这种神经传递（作用于烟碱受体）。
