Håkanson R, Böttcher G, Sundler F, Vallgren S
Digestion. 1986;35 Suppl 1:23-41. doi: 10.1159/000199380.
The stomach is rich in endocrine cells, most of which are still unidentified with respect to the peptide hormones they produce. The endocrine cell populations in the antrum usually differ from those in the oxyntic mucosa. Gastrin cells are found in the antrum and respond readily to stimuli from the gastric lumen, such as changes in the pH and the presence of food. In order to study the functional control of the antral gastrin cell, rats were subjected to different kinds of surgery. The serum gastrin concentrations in the various experimental groups were measured 8-10 weeks after the operations. Elevated antral pH raised the serum gastrin concentration. The combination of elevated antral pH and the passage of food over the pyloric glands produced gastrin cell hyperplasia. The operation that was most effective in inducing gastrin cell hyperplasia was removal of the acid-producing part of the stomach. Interestingly, gastrin cell hyperplasia was seen also after bilateral truncal vagotomy, indicating that an intact vagal innervation is not essential for the development of gastrin cell hyperplasia. Enterochromaffin-like (ECL) cells are endocrine/paracrine cells that are numerous in the acid-producing part of the stomach in many species. In the rat, they occur predominantly in the basal half of the oxyntic mucosa and produce and store histamine. The ECL cells have an unknown function and do not seem to respond to stimuli from the gastric lumen. They are activated by circulating gastrin and by vagal excitation. Gastrin mobilises histamine from these cells and activates the histamine-forming enzyme, histidine decarboxylase. Long-term hypergastrinaemia produces diffuse ECL cell hyperplasia, whereas hypogastrinaemia (following removal of the endogenous stores of gastrin by antrectomy) reduces the ECL cell number. Portacaval shunt brings about a marked increase in the number of ECL cells through an unknown mechanism. Also neuronal stimuli are important for the trophic control of the ECL cells. Studies of unilaterally vagotomised rats showed reduced weight and thickness of the oxyntic mucosa as well as a markedly reduced number of ECL cells on the denervated side. Gastric carcinoids in man are rare tumours predominantly made up of ECL cells. The incidence of such tumours is increased in patients with hypergastrinaemia (pernicious anaemia, Zollinger-Ellison syndrome). A diffuse ECL cell hyperplasia is a common finding in such patients, which is in keeping with the known gastrin sensitivity of the normal ECL cell in the rat.
胃富含内分泌细胞，其中大多数所产生的肽类激素仍未明确。胃窦部的内分泌细胞群体通常与胃体黏膜中的不同。胃泌素细胞存在于胃窦部，对来自胃腔的刺激（如pH值变化和食物的存在）反应迅速。为了研究胃窦部胃泌素细胞的功能控制，对大鼠进行了不同类型的手术。术后8 - 10周测量各实验组的血清胃泌素浓度。胃窦部pH值升高会使血清胃泌素浓度升高。胃窦部pH值升高与食物通过幽门腺相结合会导致胃泌素细胞增生。诱导胃泌素细胞增生最有效的手术是切除胃的产酸部分。有趣的是，双侧迷走神经切断术后也可见胃泌素细胞增生，这表明完整的迷走神经支配对于胃泌素细胞增生的发生并非必不可少。肠嗜铬样（ECL）细胞是内分泌/旁分泌细胞，在许多物种的胃产酸部分数量众多。在大鼠中，它们主要存在于胃体黏膜的基底部，产生并储存组胺。ECL细胞的功能尚不清楚，似乎对来自胃腔的刺激无反应。它们被循环中的胃泌素和迷走神经兴奋激活。胃泌素从这些细胞中动员组胺并激活组胺形成酶——组氨酸脱羧酶。长期高胃泌素血症会导致弥漫性ECL细胞增生，而低胃泌素血症（胃窦切除术后去除内源性胃泌素储存后）会减少ECL细胞数量。门腔分流通过未知机制使ECL细胞数量显著增加。神经刺激对ECL细胞的营养控制也很重要。对单侧迷走神经切断大鼠的研究表明，胃体黏膜的重量和厚度减少，去神经一侧的ECL细胞数量明显减少。人类胃类癌是罕见肿瘤，主要由ECL细胞组成。高胃泌素血症（恶性贫血、卓 - 艾综合征）患者中此类肿瘤的发生率增加。弥漫性ECL细胞增生在这类患者中很常见，这与大鼠正常ECL细胞已知的胃泌素敏感性相符。
