十二指肠溃疡患者抑酸治疗后壁细胞定量超微结构研究  

Quantitative Ultrastructrual Studies on Inhibited Gastric Parietal Cells

作　　者：宋军[1] 张锦坤[1] 

机构地区：[1]武汉同济医科大学附属协和医院胃肠病研究室

出　　处：《同济医科大学学报》1995年第1期36-39,共4页Acta Universitatis Medicinae Tongji

摘　　要：用洛赛克和泰胃美各治疗５例十二指肠球部溃疡，均明显抑制胃酸分泌。但洛赛克并不能使刺激型壁细胞转化为静止型，大多数壁细胞表现为病理“刺激型”结构，治疗前后壁细胞分泌小管及管泡体密度无明显变化（Ｐ＞０．０５）。泰胃美能使刺激型壁细胞转化为静止型，治疗后壁细胞分泌小管体密度明显降低（治疗前后分别为１６．７２±３．４５和４．４３±０．６２，Ｐ＜０．００１），管泡体密度明显增高（分别为４．３２±１．４５和１９．３７±３．２８，Ｐ＜０．００１）。用洛赛克治疗后，１１．２％壁细胞内可见空泡形成。这种差异是由于它们作用机制不同所致，壁细胞内分泌膜移位可能在其中起重要作用。This study was designed to compare the effects of omeprazole and tagamet on ultrastructural changes in human gastric parietal cells. Both omeprazole and tagamet remarkably inhibited active gastric acid secretion. Omeprazole, however, failed to transit an active parietal cell morphology to a resting one, in contrast to tagamet which could induced such a transition. With omeprazole, the volume densities of secretory canaliculi and tubulovesicles in parietal cells did not changes (P>0.05). For tagamet, the volume densities of secretory canaliculi markedly dropped from 16. 72±3. 45 to 4. 43±0.62and the volume densities of tubulovesicles markedly increased from 4. 32±1. 45 to 19. 37±3. 28 (P<0.001). It was noticed that omeprazole caused vacuolation in 11.2%of all parietal cells. This phenomenon was not seen in tagamet treated cases. These different findings between omeprazole and tagamet may be explained by their different inhibitory mechanisms. The secretory membrane translocation occurring in parietal cells may play an important role in it.

关 键 词：抗酸剂 十二指肠溃疡 药物疗法 超微结构 

分 类 号：R573.105[医药卫生—消化系统] R975.2[医药卫生—内科学]