Böttcher G, Håkanson R, Nilsson G, Seensalu R, Sundler F
Department of Medical Cell Research, University of Lund, Sweden.
Cell Tissue Res. 1989;256(2):247-57. doi: 10.1007/BF00218882.
The present report describes the ultrastructure of the enterochromaffin-like (ECL) cells in the stomach of the rat, hamster and guinea pig, and the ultrastructural consequences of long-term hypergastrinaemia evoked either by continuous infusion of synthetic human (Leu15)-gastrin-17 for 4 weeks (rats) or by daily treatment with large doses of the antisecretory agent omeprazole for 2-10 weeks (rats, hamsters and guinea pigs). As a result, the ECL cells increased greatly in size (maximal effect after 2 weeks of omeprazole treatment, no further gain in size after 4 or 10 weeks). Also the endoplasmic reticulum and Golgi area were enlarged. The most conspicuous feature of the ECL cells is the cytoplasmic vesicles, which are of varying size and either devoid of a dense core or with a small, often eccentrically located dense core. The vesicles probably represent the main storage site of the secretory products of the ECL cell. In addition, the cytoplasm contains granules, which differ from the vesicles in that they possess a more or less electron-dense core, surrounded by a narrow halo. The size of the vesicles ranged from small to very large, while the granules were uniformly small. Many vesicles were seen to lie very close together, some displaying an irregular outline (vacuole-like vesicles), at times giving the impression that they were undergoing fusion. The profile size (median value) of the vesicles was unaffected by gastrin infusion for 4 weeks. However, there was a tendency to a relative increase in the number of very small vesicles. In contrast, the vesicles became larger during the omeprazole treatment. Also, the number of vesicles that seemed to be engaged in fusion increased after omeprazole treatment but not after gastrin infusion. The observations support the view that ECL cells are influenced by gastrin. The effects of gastrin infusion and of omeprazole treatment on ECL cell ultrastructure were not completely identical. It cannot be excluded that the omeprazole-evoked achlorhydria evokes effects unrelated to those of hypergastrinaemia on the ECL cells, or that endogenous gastrins may evoke effects that are in some ways distinct from those of synthetic human (Leu15)-gastrin-17. Alternatively, the additional effects seen after long-term omeprazole treatment may reflect simply the duration of the hypergastrinaemic stimulus.
本报告描述了大鼠、仓鼠和豚鼠胃中肠嗜铬样（ECL）细胞的超微结构，以及通过连续输注合成人（亮氨酸15）-胃泌素-17 4周（大鼠）或每日用大剂量抗分泌剂奥美拉唑治疗2 - 10周（大鼠、仓鼠和豚鼠）所诱发的长期高胃泌素血症的超微结构后果。结果显示，ECL细胞体积大幅增大（奥美拉唑治疗2周后达到最大效应，4周或10周后体积不再进一步增大）。内质网和高尔基体区域也扩大了。ECL细胞最显著的特征是细胞质囊泡，其大小各异，要么没有致密核心，要么有一个小的、通常偏心定位的致密核心。这些囊泡可能是ECL细胞分泌产物的主要储存部位。此外，细胞质中含有颗粒，它们与囊泡的不同之处在于具有或多或少电子致密的核心，周围有一个狭窄的晕圈。囊泡的大小从小到非常大不等，而颗粒则均一较小。许多囊泡彼此靠得很近，有些呈现不规则轮廓（液泡样囊泡），有时给人一种它们正在融合的印象。囊泡的轮廓大小（中位数）不受4周胃泌素输注的影响。然而，非常小的囊泡数量有相对增加的趋势。相比之下，在奥美拉唑治疗期间囊泡变大。而且，似乎参与融合的囊泡数量在奥美拉唑治疗后增加，但在胃泌素输注后没有增加。这些观察结果支持ECL细胞受胃泌素影响的观点。胃泌素输注和奥美拉唑治疗对ECL细胞超微结构的影响并不完全相同。不能排除奥美拉唑诱发的胃酸缺乏对ECL细胞产生与高胃泌素血症无关的影响，或者内源性胃泌素可能产生在某些方面不同于合成人（亮氨酸15）-胃泌素-17的影响。或者，长期奥美拉唑治疗后出现的额外影响可能仅仅反映了高胃泌素血症刺激的持续时间。
