Stenquist B
Acta Physiol Scand Suppl. 1979;465:1-31.
Vagal activation produces a gastric acid secretory response by direct nervous stimulation of the parietal cell area and, at least in dogs, by gastrin released mainly from the antrum. In duodenal ulcer (DU) patients antrectomy reduces the acid response to sham feeding slightly more than the maximal acid output in response to pentagastrin, indicating that an antral factor contributes to the acid secretion induced by sham feeding. The marked acid response to sham feeding in antrectomized patients suggests that the direct nervous stimulation of the acid-secreting glands is the predominating stimulus in the vagal activation of acid secretion in man. In the present study vagal activation has been induced by adequate and modified sham feeding and insulin hypoglycemia in DU patients and healthy subjects. The acid response to adequate and modified sham feeding amounted to about 50% of the peak acid output in response to pentagastrin and corresponded to the acid response to an insulin dose of 0.1 U/kg b.w. Modified sham feeding seems to be a simple method of inducing physiological vagal activation of acid secretion. Sham feeding for 15 min increased only insignificantly the plasma concentrations of total gastrin immunoreactivity or heptadecapeptide gastrin. Prolonged sham feeding during intragastric neutralization or sham feeding after proximal gastric vagotomy did not significantly increase the plasma gastrin concentrations. Sham feeding is obviously a poor stimulus for release of gastrin in man. Either release effect of very small amounts of gastrin-17 or release of non-established gastrins may explain the biological effect of an antral factor. Pretreatment with benzilonium, an anticholinergic drug with minimal cerebral actions, increased the gastrin concentration after sham feeding in about half the experiments. This heterogeneous effect supports a non-cholinergic vagal release of gastrin and a cholinergic inhibition of gastrin release but also indicates a complex interaction at the level of the gastrin cells during vagal activation. Evidence for an inhibitory vagogastrone mechanism in DU patients has been found but its effect is weak and transient. Proximal gastric vagotomy abolished the acid responses to both insulin hypoglycemia and sham feeding, in accordance with the view that the direct nervous excitation of the acid-secreting glands is the predominating stimulus in the vagal activation of gastric acid secretion in man. Atropine in low doses or benzilonium inhibited the acid response to sham feeding by only 65%. This finding suggests that the direct vagal excitation of the acid-secreting glands is mediated only partially by cholinergic neurotransmission. Gastric acidification inhibited the gastric acid secretory response to insulin hypoglycemia both in healthy subjects and in DU patients. The inhibitory effect was significantly less in DU patients, however, supporting the concept of a defective inhibition by antral acidification in DU patients.
迷走神经激活通过直接神经刺激壁细胞区域产生胃酸分泌反应，并且至少在狗中，还通过主要从胃窦释放的胃泌素产生该反应。在十二指肠溃疡（DU）患者中，胃窦切除术对假饲的酸反应降低幅度略大于对五肽胃泌素的最大酸分泌量，这表明胃窦因素促成了假饲诱导的酸分泌。胃窦切除患者对假饲有明显的酸反应，这表明对泌酸腺的直接神经刺激是人类迷走神经激活酸分泌中的主要刺激因素。在本研究中，通过适当和改良的假饲以及胰岛素低血糖在DU患者和健康受试者中诱导迷走神经激活。对适当和改良假饲的酸反应相当于对五肽胃泌素的峰值酸分泌量的约50%，并且与对0.1 U/kg体重胰岛素剂量的酸反应相当。改良假饲似乎是一种诱导酸分泌生理性迷走神经激活的简单方法。假饲15分钟仅使总胃泌素免疫反应性或十七肽胃泌素的血浆浓度略有增加。胃内中和期间长时间假饲或近端胃迷走神经切断术后假饲并未显著增加血浆胃泌素浓度。显然，假饲对人类胃泌素释放是一种较弱的刺激。极少量胃泌素-17的释放效应或未确定的胃泌素的释放可能解释胃窦因素的生物学效应。用苯苄铵（一种对脑作用极小的抗胆碱能药物）预处理，在约一半的实验中增加了假饲后的胃泌素浓度。这种异质性效应支持胃泌素的非胆碱能迷走神经释放和胃泌素释放的胆碱能抑制，但也表明在迷走神经激活期间胃泌素细胞水平存在复杂的相互作用。已发现DU患者中存在抑制性迷走抑胃素机制的证据，但其作用微弱且短暂。近端胃迷走神经切断术消除了对胰岛素低血糖和假饲的酸反应，这与以下观点一致，即对泌酸腺的直接神经兴奋是人类迷走神经激活胃酸分泌中的主要刺激因素。低剂量阿托品或苯苄铵仅抑制了65%的假饲酸反应。这一发现表明，对泌酸腺的直接迷走神经兴奋仅部分由胆碱能神经传递介导。胃酸化在健康受试者和DU患者中均抑制了对胰岛素低血糖的胃酸分泌反应。然而，在DU患者中抑制作用明显较小，这支持了DU患者中胃窦酸化抑制缺陷的概念。
