Ribet A, Balas D, Bastie M J, Senegas-Balas F, Escourrou J, Bommelaer G, Pradayrol L
Scand J Gastroenterol Suppl. 1981;70:155-74.
Cytological effects of two H2-receptor antagonists on the gastric and duodenal mucosa were studied during therapy of active duodenal ulcer (D.U.) in man. After endoscopic diagnosis (day 0), subjects were treated with cimetidine or ranitidine and re-examined on day 30. Only subjects with healed D.U. on day 30 were retained in this study. Gastric, pyloric and duodenal endoscopic biopsies were taken and treated for further morphometrical analysis both by light and electron microscopy. The use of the immunoperoxidase technique allowed evaluation of G and D cell populations. Kinetic parameters in proliferative zones were measured after in vitro incubation of biopsies with 3H-thymidine. No differences could be seen between the two H2-receptor antagonists. Increase of tubulovesicles and decrease of canaliculi in parietal cells are closely related to the inhibitory effect of these drugs on acid secretion. However secretory capacities of parietal cells are preserved since the whole membrane (tubulovesicle + canaliculi surface) remained constant. The collapsed aspect of the tubulovesicles on day 30 and the presence of connections between the tubulovesicle membrane, with both vesicle and canaliculi membrane, could support the theory of osmotic membrane expansion during parietal cell acid secretion. H2-receptor antagonists have been shown to be trophic in duodenal mucosa: both villi and microvilli area are increased. Confirming these findings, the proliferative compartment in the intestinal crypts was shown to be enlarged. No variation of G cell number could be seen in the antral mucosa; clear intracytoplasmic granules were increased in D.U. on day 0 but were not further modified on day 30. Somatostatin labelling index decreased. These last findings associated with the lack of G cell variations, suggest the presence of a possible paracrine modulation in the gastric and duodenal mucosa.
在人类活动性十二指肠溃疡（D.U.）治疗期间，研究了两种H2受体拮抗剂对胃和十二指肠黏膜的细胞学效应。在内镜诊断后（第0天），受试者接受西咪替丁或雷尼替丁治疗，并在第30天进行复查。本研究仅纳入第30天时十二指肠溃疡已愈合的受试者。采集胃、幽门和十二指肠的内镜活检组织，通过光学显微镜和电子显微镜进行进一步的形态计量分析。采用免疫过氧化物酶技术评估G细胞和D细胞群体。将活检组织与3H-胸腺嘧啶核苷进行体外孵育后，测量增殖区的动力学参数。两种H2受体拮抗剂之间未见差异。壁细胞内微管泡增加和细胞内小管减少与这些药物对胃酸分泌的抑制作用密切相关。然而，壁细胞的分泌能力得以保留，因为整个膜（微管泡+小管表面）保持恒定。第30天时微管泡的塌陷状态以及微管泡膜与囊泡膜和小管膜之间存在连接，可能支持壁细胞胃酸分泌过程中渗透膜扩张的理论。已证明H2受体拮抗剂对十二指肠黏膜具有营养作用：绒毛和微绒毛面积均增加。证实这些发现的是，肠道隐窝中的增殖区增大。胃窦黏膜中G细胞数量未见变化；第0天时十二指肠溃疡中清晰的胞质内颗粒增加，但在第30天时未进一步改变。生长抑素标记指数降低。这些最后的发现与G细胞无变化相关，提示胃和十二指肠黏膜中可能存在旁分泌调节。
