Rasmussen L, Oster-Jørgensen E, Qvist N, Pedersen S A
Dept. of Surgical Gastroenterology, Odense University Hospital, Denmark.
Scand J Gastroenterol. 1999 Jul;34(7):671-5. doi: 10.1080/003655299750025868.
The present study was designed to investigate whether omeprazole changes the characteristics and thereby the functions ascribed to fasting intestinal motility, postprandial motility, postprandial pH, and gastric emptying.
Ten healthy subjects were investigated. The studies were performed after 10 days of treatment with 40 mg omeprazole daily/placebo. Duodenal pressures and intragastric pH were detected by strain-gauge transducers and a pH electrode attached to a miniature computer. The meal consisted of an omelette labelled with 99mTc-sulphur colloids followed by 150 ml water labelled with 111In-diethylenetriamine pentaacetic acid.
The difference in fasting intragastric pH between the two series was highly significant. The profile from the placebo series showed a relationship between phase activity and pH. The pH increased from phase I (median, 1.3; 95% confidence interval (CI), 0.9-1.6) to a maximum at 25% (1.8 (0.9-2.1)) and 50% (1.6 (1.1-3.8)) of cycle duration and decreased thereafter until the end of the cycle. The profile from the omeprazole series showed significantly higher values during the entire cycle but no relationship between phase activity and pH. Pretreatment with omeprazole was followed by a delay in gastric emptying of liquid at 30 min (64% (49%-66%) (omeprazole series) versus 78% (67%-83%); P < 0.01) and solid at 180 min (71% (48%-86%) (omeprazole series) versus 96% (87%-100%); P < 0.01). There was no significant difference in duration of postprandial motility (305 min (157-350 min) (omeprazole) versus 259 min (129-403 min)).
Omeprazole eliminates the temporal relationship between intragastric pH and characteristics of the migrating motor complex and induces a delay in gastric emptying of both liquid and solid. A non-significant increase in duration of postprandial motility may represent a type-II error.
本研究旨在调查奥美拉唑是否会改变空腹肠道动力、餐后动力、餐后pH值和胃排空的特征及相应功能。
对10名健康受试者进行研究。在每日服用40毫克奥美拉唑/安慰剂治疗10天后进行各项研究。十二指肠压力和胃内pH值通过应变片传感器和连接微型计算机的pH电极进行检测。餐食包括用99mTc-硫胶体标记的煎蛋卷,随后是用111In-二乙三胺五乙酸标记的150毫升水。
两个系列空腹胃内pH值的差异非常显著。安慰剂系列的曲线显示了相活动与pH值之间的关系。pH值从第一阶段(中位数,1.3;95%置信区间(CI),0.9 - 1.6)开始升高,在周期持续时间的25%(1.8(0.9 - 2.1))和50%(1.6(1.1 - 3.8))时达到最大值,此后下降直至周期结束。奥美拉唑系列的曲线在整个周期内显示出显著更高的值,但相活动与pH值之间没有关系。服用奥美拉唑预处理后,液体在30分钟时胃排空延迟(奥美拉唑系列为64%(49% - 66%),而安慰剂系列为78%(67% - 83%);P < 0.01),固体在180分钟时胃排空延迟(奥美拉唑系列为71%(48% - 86%),而安慰剂系列为96%(87% - 100%);P < 0.01)。餐后动力持续时间没有显著差异(奥美拉唑组为305分钟(157 - 350分钟),安慰剂组为259分钟(129 - 403分钟))。
奥美拉唑消除了胃内pH值与移行性运动复合波特征之间的时间关系,并导致液体和固体的胃排空延迟。餐后动力持续时间的非显著增加可能代表II类错误。