Thompson J N, Barr J A, Collier N, Spencer J, Bush A, Cope L, Gribble R J, Baron J H
Gut. 1985 Oct;26(10):1018-24. doi: 10.1136/gut.26.10.1018.
Gastric secretion was measured in nine patients with duodenal ulcer before, and after treatment for four weeks with omeprazole 20 mg or 40 mg daily. Basal acidity and acid output were affected variably by 20 mg, but inhibited totally by 40 mg daily. Sham feed stimulated acid output was reduced by 20 mg daily and completely inhibited by 40 mg daily. Maximal pentagastrin stimulated acid output was halved by 20 mg omeprazole daily and 84% inhibited by 40 mg daily. The reduction in acidity was always greater than the reduction of volume. Pepsin output after pentagastrin was little altered but with the reduced secretory volume pepsin concentrations were increased by both doses. The major cause of reduced aspirate acid output after omeprazole is decreased secretion of the primary acid component of the parietal cell by the proton pump H+K+ ATPase. Duodenogastric alkaline reflux is, however, markedly increased after omeprazole and is an additional factor in the resultant hypoacidity or even anacidity after this drug.
对9例十二指肠溃疡患者在服用每日20毫克或40毫克奥美拉唑治疗四周前后进行胃液分泌测定。基础酸度和酸分泌量受20毫克剂量影响各异，但每日40毫克可完全抑制。假饲刺激的酸分泌量每日20毫克时减少，每日40毫克时完全抑制。最大五肽胃泌素刺激的酸分泌量每日20毫克奥美拉唑时减半，每日40毫克时抑制84%。酸度的降低总是大于分泌量的减少。五肽胃泌素刺激后的胃蛋白酶分泌量变化不大，但由于分泌量减少，两种剂量均使胃蛋白酶浓度升高。奥美拉唑后抽吸胃酸分泌量减少的主要原因是质子泵H⁺K⁺ATP酶使壁细胞的主要酸成分分泌减少。然而，奥美拉唑后十二指肠-胃碱性反流明显增加，是该药物导致胃酸过少甚至无酸状态的另一个因素。
