Hui W M, Liu H C, Lam S K
Department of Medicine, Queen Mary Hospital, University of Hong Kong.
J Gastroenterol Hepatol. 1989 Mar-Apr;4(2):143-9. doi: 10.1111/j.1440-1746.1989.tb00818.x.
H2-Receptor antagonists and omeprazole, a H-K ATPase inhibitor, inhibit acid secretion from the parietal cells. The ultrastructural changes of the parietal cells after treatment have been described, but the changes in the mitochondrial activity which reflect the energetic metabolism were not well defined. To study the effect of omeprazole and H2-receptor antagonists on the mitochondrial activity of the parietal cells, endoscopic biopsies were taken from nine patients with duodenal ulcer before and after treatment with either 10 mg or 20 mg omeprazole each morning, or 150 mg ranitidine twice daily for 2 weeks, given in a double-blind randomized manner. Three patients with healed duodenal ulcer who were on maintainence treatment with 150 mg ranitidine nightly for 1 year had an endoscopy performed after 4 and 12 months and two non-ulcer dyspeptic patients were recruited as controls. Three biopsies were taken during each endoscopy from the body of the stomach. The mitochondrial activity was assessed by the reaction of succinic dehydrogenase with nitroblue tetrazolium and of cytochrome oxidase with naphthoic acid mixed with N-phenyl-p-phenylenediamine, according to the intensity of the staining reaction. After treatment with omeprazole or ranitidine, the mitochondrial activity decreased appreciably and returned to the pretreatment level on cessation of treatment. Patients on maintainence ranitidine showed decreased mitochondrial activities after 4 months, which, however, returned to pretreatment levels in two patients. It is concluded that short-term treatment with omeprazole or ranitidine resulted in reversible suppression of mitochondrial activity while long-term treatment with ranitidine resulted in an initial suppression followed by a tendency to return to pretreatment level despite continued treatment.
H2受体拮抗剂和质子泵抑制剂奥美拉唑可抑制壁细胞分泌胃酸。此前已有关于治疗后壁细胞超微结构变化的描述，但反映能量代谢的线粒体活性变化尚不明确。为研究奥美拉唑和H2受体拮抗剂对壁细胞线粒体活性的影响，对9例十二指肠溃疡患者进行了内镜活检，这些患者分别接受每日晨起10毫克或20毫克奥美拉唑治疗，或每日两次、每次150毫克雷尼替丁治疗，为期2周，治疗前后均进行活检，采用双盲随机方式给药。3例十二指肠溃疡已愈合且每晚服用150毫克雷尼替丁维持治疗1年的患者，分别在4个月和12个月后接受内镜检查，并招募2例非溃疡性消化不良患者作为对照。每次内镜检查时从胃体部取3块活检组织。根据染色反应强度，通过琥珀酸脱氢酶与硝基蓝四氮唑的反应以及细胞色素氧化酶与萘酸混合N-苯基对苯二胺的反应来评估线粒体活性。使用奥美拉唑或雷尼替丁治疗后，线粒体活性明显降低，停止治疗后恢复到治疗前水平。服用维持量雷尼替丁的患者在4个月后线粒体活性降低，但其中2例患者的线粒体活性在继续治疗过程中恢复到治疗前水平。结论是，短期使用奥美拉唑或雷尼替丁会导致线粒体活性可逆性抑制，而长期使用雷尼替丁则会导致初始抑制，尽管继续治疗，但随后有恢复到治疗前水平的趋势。
