McLoughlin J C, Hayes J R, Buchanan K D, Kelly J G
Gut. 1978 Jul;19(7):632-9. doi: 10.1136/gut.19.7.632.
Both vagal and sympathetic innervation been have described as influencing hormone release from the gastrointestinal tract and pancreas. The role of neural influences on the release of gastrin, glucagon, and secretin has been studied using the potent autonomic nerve stimulus of hypoglycaemia. Healthy subjects were each rendered hypoglycaemic by insulin 0.2 units/kg on three occasions: after atropine 20 microgram/kg: after propranolol 160 mg orally, and without prior drug administration. Adequate beta-blockade was confirmed by observation of the pusle rate response to a standard exercise at the end of the experiment, and by measurements of plasma propranolol levels. Hypoglycaemia failed to produce a rise in plasma gastrin under either propranolol or control conditions but a significant rise was noted with prior atropinisation. The glucagon response to hypoglycaemia, when measured with either the C- or N-terminal reactive antibodies, was found not to be influenced to any significant extent by either beta-blockade or atropinisation. No alteration in plasma secretin levels was noted during hypoglycaemia. It therefore appears that neural influences are relatively unimportant in the release of gastrin, glucagon, and secretin in man.
迷走神经和交感神经支配均被描述为影响胃肠道和胰腺的激素释放。利用低血糖这种强大的自主神经刺激,对神经影响胃泌素、胰高血糖素和促胰液素释放的作用进行了研究。健康受试者在三种情况下分别通过注射0.2单位/千克胰岛素导致低血糖:一次在注射20微克/千克阿托品后;一次在口服160毫克普萘洛尔后;还有一次未预先给药。在实验结束时,通过观察对标准运动的脉搏率反应以及测量血浆普萘洛尔水平,确认了充分的β受体阻滞。在普萘洛尔或对照条件下,低血糖均未能使血浆胃泌素升高,但在预先给予阿托品后,血浆胃泌素显著升高。当用C末端或N末端反应性抗体测量时,发现低血糖引起的胰高血糖素反应在很大程度上不受β受体阻滞或阿托品化的影响。低血糖期间血浆促胰液素水平未发生变化。因此,在人类中,神经影响在胃泌素、胰高血糖素和促胰液素的释放中似乎相对不重要。