酸抑制对胃内分泌细胞的影响。

Effect of acid inhibition on gastric endocrine cells.

作者信息

Arnold R, Koop H, Schwarting H, Tuch K, Willemer B

出版信息

Scand J Gastroenterol Suppl. 1986;125:14-9. doi: 10.3109/00365528609093813.

Abstract

There is increasing evidence that the numbers of antral G cells and of fundic argyrophil (ECL) cells are influenced by agents that inhibit gastric acid secretion. Antral G cells increase in states of achlorhydria in man and animals provided atrophic antral gastritis is absent. In rats, treatment with substituted benzimidazoles like omeprazole and BY 308 increase G-cell densities dose-dependently. Even high doses of histamine H-2 antagonists and antacids increase antral G-cell densities. In contrast to G cells, antral D cells decrease in these instances. Fundic ECL cells increase in all experimental conditions of complete achlorhydria provided intact antral mucosa is present, i.e. there is elevated serum gastrin. Antacid treatment is not followed by an increase of fundic ECL cells, which could be explained by the less sustained increase of serum gastrin.

摘要

越来越多的证据表明，胃窦G细胞和胃底嗜银（ECL）细胞的数量受抑制胃酸分泌的药物影响。在人和动物无萎缩性胃窦炎的胃酸缺乏状态下，胃窦G细胞数量增加。在大鼠中，用奥美拉唑和BY 308等取代苯并咪唑治疗可使G细胞密度呈剂量依赖性增加。即使是高剂量的组胺H2拮抗剂和抗酸剂也会增加胃窦G细胞密度。与G细胞相反，在这些情况下胃窦D细胞减少。在所有完全胃酸缺乏的实验条件下，只要胃窦黏膜完整，即血清胃泌素升高，胃底ECL细胞就会增加。抗酸治疗后胃底ECL细胞不会增加，这可以用血清胃泌素升高持续时间较短来解释。