Single-dose oral omeprazole for reduction of gastric residual acidity in adults for outpatient surgery

Omeprazole is a substituted benzimidazole that causes dose-dependent intracellular inhibition of gastric acid secretion in humans. This double-blind study examined the effect of omeprazole in decreasing gastric acidity and gastric residual volume in outpatient adults. Unpremedicated outpatients, ASA I-III, 18 years or older (n = 17), were randomly assigned to receive omeprazole 80 mg, or placebo by mouth the night before scheduled elective outpatient surgery. The patients were fasted for 8 h prior to surgery. After the patient was anesthetized, an orogastric tube was inserted with proper placement verified by auscultation for gastric sounds. Gastric residual contents were withdrawn into a Luken's trap, and pH was then determined and gastric volume indexed to weight (ml.kg-1). Data were analyzed by a t-test, with P less than 0.05 considered statistically significant. Patient characteristics of both groups were similar. There was a statistically significant difference between the two groups for pH (P = 0.02), but not between the two groups for gastric volume indexed to weight (P = 0.07).     

埃索美拉唑三联与奥美拉唑三联疗法治疗Hp阳性十二指肠溃疡对比研究

目的比较埃索美拉唑三联与奥美拉唑三联疗法治疗幽门螺杆菌（Hp）阳性十二指肠球部溃疡的临床疗效。方法将104例经内镜诊断并检测证实Hp阳性的十二指肠球部溃疡患者随机分为两组。埃索美拉唑组（52例）：埃索美托唑20mg＋阿莫西林1g＋克托霉素500mg，每日2次，共7d；奥美拉唑组（52例）：奥美拉唑20mg＋阿莫西林1g＋克拉霉素500mg，每日2次，共7d。疗程结束4周后复查胃镜并检测Hp，观察腹痛缓解率、溃疡愈合率、Hp根除率及用药后的不良反应等。结果埃索美拉唑组第1天和第2天腹痛缓解率分别为34．6％和59、6％，高于奥美托唑组的17.3％和38．5％（P〈0．05）。埃索美托唑组和奥美拉唑组溃疡愈合率分别为92.3％和88．5％，Hp根除率分别为88．5％和82．7％，差异无显著性（P〉0．05）。两组用药后不良反应少，有较好的安全性。结论埃索美拉唑三联疗法治疗Hp阳性的十二指肠溃疡安全有效．腹痛缓解速度优于奥美拉唑三联疗法。     

Effect of Omeprazole on Diazepam Disposition in the Rat: in Vitro and in Vivo Studies

Purpose. The inhibitory effects of omeprazole on diazepam metabolism in vitro and in vivo are compared in the rat. Methods. 3-hydroxylation and N-demethylation of diazepam was investigated in the presence of a range of omeprazole concentrations (2-500µM) in hepatic microsomes and hepatocytes. Zero order infusions together with matched bolus doses of omeprazole were used to achieve a range of steady state plasma concentrations (10-50mg/ L) and to study the diazepam-omeprazole interaction in vivo. Results. The 3-hydroxlation pathway was more prone to inhibition (K_Is 108 ± 30 and 28 ± 11 µM in microsomes and hepatocytes, respectively) than the demethylation pathway (K_Is of 226 ± 76 and 59 ± 27 µM in microsomes and hepatocytes, respectively). In both in vitro systems, the mechanism of inhibition was competitive with Km/K_I ratios larger than 1 for the 3HDZ pathway and smaller than 1 for the NDZ pathway. There was an omeprazole concentration dependent decrease in diazepam clearance in vivo which could be modelled using a simple inhibition equation with a K_I of 57µM (19.8mg/L). In contrast there was no statistically significant change in the steady state volume of distribution for diazepam in the presence of omeprazole. Conclusions. The in vivo K_I for the omeprazole: diazepam inhibition interaction shows closer agreement with the K_I values obtained in hepatocytes than with those observed in microsomes.     

Effect of single-dose omeprazole and ranitidine on gastric juice acidity and volume in patients undergoing laparotomy

The effects of oral omeprazole and oral ranitidine on gastric fluid volume and pH were compared in 95 elective surgical patients, randomly assigned to one of three groups. The patients received either 80 mg of omeprazole or 300 mg of ranitidine orally at 6.00 on the morning of surgery. One third of the patients received no antacid therapy. Following induction, a no. 18 nasogastric tube was passed into the stomach and all available gastric fluid was aspirated. pH and volumes were measured. In the omeprazole- and ranitidine-treated groups, the mean pH was > 5.4 after induction, at completion of surgery and 1 h after operation, although at least one patient in both groups had pH < 2.5. The volumes of gastric aspirates were reduced equally by both drugs. Two patients in the omeprazole group, none in the ranitidine group and eight in the control group (26%) had pH <2.5 with volume> 25 ml at induction. Both drugs appeared to be effective in reducing the volume of intragastric fluid and acidity to acceptable values.     

In vivo and in vitro studies of the site of inhibitory action of omeprazole on adrenocortical steroidogenesis

Summary The site of omeprazole inhibition of adrenal steroidogenesis has been sought in vivo by analyzing the patterns of urinary steroid metabolite excretion after 6 days of treatment with placebo/omeprazole.Excretion rates of androsterone, aetiocholanolone, dehydroepiandrosterone, 11 hydroxyandrosterone, tetrahydrocortisone, tetrahydrocortisol and cortolone were reduced, indicating a block at an early step in steroidogenesis, possibly cholesterol side-chain cleavage. In vitro studies have confirmed this finding by measuring conversion of added precursors to cortisol in isolated bovine adrenocortical cells. Cortisol synthesis from added 20 hydroxycholesterol was inhibited by 83% in the presence of 100 µg omeprazole/ml. Conversion from pregnenolone and progesterone and their 17 hydroxylated derivatives was inhibited by 20–40% whereas cortisol production from added 11 deoxycortisol was not affected.These data suggest that omeprazole primarily inhibits cholesterol cleavage and does not inhibit 3 hydroxysteroid dehydrogenase, 17 hydroxylase or 11 hydroxylation; 21 hydroxylase activity may be marginally attenuated.     

康复新液联合奥美拉唑对HP阴性胃溃疡的疗效分析

目的分析康复新液联合奥美拉唑治疗幽门螺杆菌(HP)阴性胃溃疡患者的疗效。 方法选取HP阴性胃溃疡患者108例,随机均分为对照组和联合组。对照组接受奥美拉唑针剂治疗,联合组接受康复新液联合奥美拉唑针剂治疗。比较两组临床疗效、血清胃蛋白酶原(PG)、高迁移率族蛋白B1(HMGB1)、细胞炎症因子水平及不良反应发生率。 结果联合组治疗总有效率高于对照组(P＜0.05)。与治疗前比较,两组治疗后PGⅠ、PGⅡ、HMGB1、白细胞介素-6、肿瘤坏死因子-α及C反应蛋白均有降低,且联合组较对照组降低更明显(P＜0.05)。两组患者治疗期间总不良反应发生率比较,差异无统计学意义(P＞0.05)。 结论康复新液联合奥美拉唑针剂可提高HP阴性胃溃疡患者的临床疗效,值得临床应用推广。     

奥美拉唑对家兔肾脏内髓集合管细胞H+/K+交换功能的影响

目的探讨奥美拉唑对家兔肾脏IMCD细胞H+/K+交换的影响,以及经洗涤处理是否解除这种影响.方法原代培养家兔肾脏IMCD细胞单层,在100 μmol/L奥美拉唑缓冲液中孵育25 min, 洗涤组则在奥美拉唑缓冲液孵育后,用不含奥美拉唑的缓冲液洗涤IMCD细胞;对照组在不含奥美拉唑的缓冲液孵育25 min;CECF/AM荧光探针法测定各组IMCD细胞H+/K+交换.结果奥美拉唑组的H+/K+交换为(0.016±0.006) dpHi/min(n=8);与对照组的(0.053±0.008) dpHi/min(n=8)相比,相差非常显著(P<0.001);洗涤组的H+/K+交换为(0.016±0.006) dpHi/min(n=6),与对照组(n=6)的(0.052±0.009)dpHi/min相比,相差非常显著(P<0.001).结论 100 mol/L的奥美拉唑对家兔IMCD细胞的H+/K+交换有显著影响,而且洗涤处理不能解除这种抑制.因而,肺心病合并上消化道出血患者使用奥美拉唑时,应综合考虑其利弊.     

奥美拉唑和西咪替丁治疗危重病儿应激性溃疡出血的随机对照试验

目的 :探讨奥美拉唑治疗危重病儿应激性溃疡出血的临床疗效。方法 :将 82例应激性溃疡出血的危重病儿随机分为奥美拉唑治疗组 4 7例 [男性2 5例 ,女性 2 2例 ,年龄 (6±s 3)a]和对照组 35例[男性 19例 ,女性 16例 ,年龄 (5 .9± 2 .8)a]。 2组均给予病因、对症及支持治疗 ,同时治疗组给予奥美拉唑 0 .6～ 0 .8mg·kg- 1,每日 1次口服或经胃管注入 ,连用 3～ 5d。对照组给予西咪替丁每日 10～ 2 0mg·kg- 1,静脉输注 ,连用 3～ 5d。观察应激性溃疡出血临床好转情况 ,同时观察不良反应的发生情况。结果 :奥美拉唑治疗组 ,显效 4 2 % ,有效 4 7% ,无效11% ,总有效 89% ;对照组 ,显效 14% ,有效4 6% ,无效 4 0 % ,总有效 60 % ,2组相比差异有非常显著的意义 (P <0 .0 1)。结论 :奥美拉唑治疗危重病儿应激性溃疡出血疗效显著 ,且不良反应少     

消化性溃疡的病因和药物治疗

消化性溃疡是我国人群中常见病之一 ,各种因素如幽门螺杆菌感染、药物、遗传及社会心理因素等均可诱发或促进本病的发生。组胺H2 受体拮抗剂如法莫替丁、尼扎替丁等和质子泵抑制剂如奥美拉唑、兰索拉唑等抗酸分泌药物与胃粘膜保护剂如硫糖铝混悬液、胶态次枸椽酸铋等联合应用可有效的治疗消化性溃疡病。应用奥美拉唑、阿莫西林及克拉霉素三联 7d治疗可有效的根治幽门螺杆菌和促进溃疡愈合     

奥美拉唑联合雷尼替丁治疗十二指肠溃疡的抑酸疗效分析

目的:比较奥美拉唑(omeprazole,OME)不同剂量及联合雷尼替丁(ranitidine,RAN)治疗十二指肠球部溃疡(duodenal uncler,DU)活动期患者的抑酸效果,特别是对夜间酸突破(noctumal acid breakthrough,NAB)现象的控制,并探讨幽门螺杆菌(helicobacter pylori,HP)对抑酸疗效的影响.方法:病例选自经本院胃镜确诊为十二指肠球部溃疡活动期患者74例,随机分配入4个治疗组:A组,13例,OME 20 mg每天1次;B组,37例,OME 20 mg每天2次;C组,11例,OME 40 mg静脉推注,每12 h 1次;D组,13例,B方案联合RAN 150 mg睡前口服.在第5天对入组病人进行24 h胃内pH监测.结果:4组胃内24 h及夜间平均pH值、中位pH值、pH＜4所占的时段百分比及NAB发生率(A组76.9%,B组24.3%,C组18.2%,D组7.7%)差异有显著性,其中,A组与B、C、D 3组差异有显著性(P＜0.001);B、C、D 3组比较差异无显著性(P＞0.05);同一治疗组内HP阳性者24 h及夜间平均pH值、中位pH值均高于阴性者,pH＜4所占的时段百分比低于阴性者.HP阳性者NAB发生率低于阴性组(13.7%vs44.1%,P＜0.05),而在4个治疗组内仅有A组内HP阳性者NAB发生率低于阴性者,其余3组HP感染与否对NAB发生率无影响.结论:OME抑酸疗效具有剂量依赖效应,联用RAN有减少NAB的趋势.HP感染者应用OME抑酸效果较好.