Chen D, Zhao C M, Andersson K, Sundler F, Håkanson R
Department of Pharmacology, University of Lund, Sölvegatan 10, S-22362 Lund, Sweden.
Cell Tissue Res. 1996 Mar;283(3):469-78. doi: 10.1007/s004410050558.
Histamine-producing enterochromaffin-like (ECL) cells are numerous in the oxyntic mucosa of the rat stomach. They respond to gastrin by secretory activation, hypertrophy and hyperplasia. They contain cytoplasmic granules (median profile diameter 120 nm), secretory vesicles (180 nm) and microvesicles (70 nm). alpha-Fluoromethylhistidine (alpha-FMH) depletes histamine from the ECL cells by inhibiting the histamine-forming enzyme histidine decarboxylase. Long-term hypergastrinemia, evoked by omeprazole, increases the ECL-cell histamine concentration. The way in which chronic histamine depletion affects omeprazole-induced ECL-cell hypertrophy, and the ways in which granules and vesicles in the ECL cells respond to alpha-FMH and/or omeprazole have been studied. Rats were treated with alpha-FMH (3 mg/kg per h subcutaneously), omeprazole (400 micromol/kg per day orally), alpha-FMH+omeprazole, or vehicle for 6 weeks. ECL cell profiles in electron micrographs were analysed panimetrically. The results show that the omeprazole-evoked hypertrophy of the ECL cells is not affected by depletion of ECL-cell histamine, thereby supporting the view that ECL-cell histamine is not important for full expression of the gastrin-evoked trophic effects on the ECL cells. The loss of ECL-cell histamine following treatment with alpha-FMH and with alpha-FMH+omeprazole is associated with a greatly reduced size of the secretory vesicle compartment. The granules, on the other hand, are unaffected by alpha-FMH and alpha-FMH+omeprazole. Omeprazole treatment leads to the appearance of numerous vacuoles (with profile diameter greater than 500 nm); such vacuoles are not observed in the ECL cells of rats treated with alpha-FMH or alpha-FMH+omeprazole. The omeprazole-induced increase in ECL-cell histamine is associated with an increase in the compartment composed of secretory vesicles and vacuoles. The findings support the hypothesis that secretory vesicles (and vacuoles) represent a major storage site of ECL-cell histamine.
产生组胺的肠嗜铬样（ECL）细胞在大鼠胃的泌酸黏膜中数量众多。它们通过分泌激活、肥大和增生对胃泌素作出反应。它们含有细胞质颗粒（平均轮廓直径120纳米）、分泌囊泡（180纳米）和微囊泡（70纳米）。α-氟甲基组氨酸（α-FMH）通过抑制组胺形成酶组氨酸脱羧酶，使ECL细胞中的组胺耗竭。奥美拉唑诱发的长期高胃泌素血症会增加ECL细胞的组胺浓度。研究了慢性组胺耗竭对奥美拉唑诱导的ECL细胞肥大的影响方式，以及ECL细胞中的颗粒和囊泡对α-FMH和/或奥美拉唑的反应方式。给大鼠皮下注射α-FMH（每小时3毫克/千克）、口服奥美拉唑（每天400微摩尔/千克）、α-FMH+奥美拉唑或赋形剂，持续6周。对电子显微镜照片中的ECL细胞轮廓进行全景分析。结果表明，奥美拉唑诱发的ECL细胞肥大不受ECL细胞组胺耗竭的影响，从而支持了ECL细胞组胺对于胃泌素对ECL细胞诱发的营养作用的充分表达不重要这一观点。用α-FMH和α-FMH+奥美拉唑处理后，ECL细胞组胺的丧失与分泌囊泡区室大小的大幅减小有关。另一方面，颗粒不受α-FMH和α-FMH+奥美拉唑的影响。奥美拉唑处理导致出现大量空泡（轮廓直径大于500纳米）；在用α-FMH或α-FMH+奥美拉唑处理的大鼠的ECL细胞中未观察到此类空泡。奥美拉唑诱导的ECL细胞组胺增加与由分泌囊泡和空泡组成的区室增加有关。这些发现支持了分泌囊泡（和空泡）代表ECL细胞组胺主要储存部位的假说。
