胃电振幅与胃运动间相关性的研究

在28例功能性消化不良(FD)患者和13例健康人,进行了胃电描记和胃窦测压,探讨体表胃电图(EGG)的振幅与胃动力间的相关性。记录空腹胃动力3.5小时,餐后胃动力1.5小时,于移行运动复合波(MMC)的每一期及餐后记录EGG。在8例FD患者,于MMC的Ⅰ期静滴红霉素200mg,滴速为6.6mg/min,滴注期间记录EGG。结果表明;空腹胃电振幅在MMC的Ⅲ期最高,Ⅰ期最低(P<0.01);在静滴红霉素期间,胃窦收缩的频率、强度、动力指数(MI)和胃电振幅均较静滴前显著增加(P<0.01);在7例FD,餐后胃窦MI低于正常;在9例FD,餐后MI正常;餐后胃电振幅在动力减低的FD患者显著低于动力正常的FD(P<0.01)。结论:胃电振幅与胃平滑肌机械收缩有关,高电振幅伴随强收缩活动,胃电振幅有可能成为反映胃动力的指标。     

乙醇对犬消化间期及餐后胃和十二指肠收缩的影响

为了探讨饮酒引起消化不良的机理 ,本文应用低顺应性毛细管水灌注消化道腔内测压系统记录清醒犬胃和十二指肠收缩活动并在犬消化间期胃肠移行性复合运动 (MMC)不同时相抽取静脉血 ,观察胃内灌流乙醇对MMC和餐后胃肠运动的作用及血浆胃动素浓度变化 .结果表明 :①在MMCⅡ相后期从胃管内灌流 15 %乙醇延长了MMC周期时间 ,灌流乙醇后出现的MMCⅢ相收缩时间 ,振幅和动力指数明显低于正常对照灌流 30 %乙醇则抑制了MMCⅢ相出现 .②血浆胃动素随MMC不同时相呈周期性波动 ,血浆胃动素浓度在MMCⅢ相时最高 ,MMCⅠ相时最低 .在灌流 15 %乙醇后出现MMCⅢ相时 ,血浆胃动素高峰浓度降低 .灌流 30 %乙醇则抑制了消化间期血浆胃动素浓度高峰出现 .③在犬进餐后灌流 30 %乙醇明显抑制了餐后胃和十二指肠的收缩活动 .因此 ,胃内灌流乙醇减弱了犬消化间期和餐后胃和十二指肠的收缩 ,血浆胃动素释放减少可能部分介导了乙醇的胃肠抑制作用 .结果提示这可能是饮酒引起临床消化不良的原因 .     

红霉素对狗消化间期和餐后胃肠运动的影响及机制探讨

目的观察静脉注射红霉素对狗消化间期胃肠移行性复合运动（ＭＭＣ）和餐后运动的作用并探讨可能机制。方法应用低顺应性毛细管水灌注消化道腔内测压系统记录清醒狗胃肠收缩活动。在ＭＭＣＩ相和餐后静脉注射红霉素记录胃肠运动变化并抽血测定血浆胃动素浓度。结果①血浆胃动素随ＭＭＣ不同时相呈周期性波动,血浆胃动素浓度在 ＭＭＣⅢ相时最高,ＭＭＣＩ相时最低。②在 ＭＭＣＩ相时从静脉注射红霉素可以激发胃和十二指肠ＭＭＣⅢ相收缩,但不伴有血浆胃动素升高。引起狗ＭＭＣⅢ相收缩的最适红霉素浓度为０,５ｍｇ·ｋｇ－１体重;红霉素１０ｍｇ·ｋｇ－１引起胃肠持续收缩并出现十二指肠－胃逆蠕动,导致恶心呕吐。③阿托品明显抑制红霉素所致的胃和十二指肠ＭＭＣⅢ相收缩。④红霉素增强狗餐后胃窦和十二指肠的收缩活动。结论红霉素有促进胃肠动力作用,作用机制与胃动素释放无关,可能部分通过胆碱能神经介导。     

十二指肠溃疡的胃十二指肠动力学特征

为探讨十二指肠溃疡(Du)患者胃十二指肠动力学特征,本文对Du及健康志愿者共23例进行消化间期及消化期胃十二指肠压力测定,并对动力参数及消化间期复合运动(IDMC)Ⅲ期的特征加以分析。     

体表胃电频谱与消化间期复合运动的关系

为探讨体表胃电(EGG)与胃肠动力相互关系,了解空腹状态下消化间期复合运动(IDMC)不同时期的胃电频谱变化,本文对慢性胃病患者同步进行3小时消化间期胃及十二指肠压力及EGG测定,并对主频、振幅与胃动力之间关系加以讨论。 1 材料和方法 1.1 研究对象 20例非溃疡性消化不良(NuD)及8例十二指肠溃疡均经电子胃镜、     

胃癌全胃切除术后Roux肠袢运动变化的研究

目的通过对胃癌全胃切除、食管空肠Roux-Y吻合术后患者进行Roux空肠袢动力测定，探讨RouxY综合征的发病机制。方法全胃切除、Roux-Y食管空肠重建术后6～12个月，通过7通道测压导管监测Roux空肠袢在消化间期及消化期的压力变化。结果Roux肠袢消化间期缺乏移行性复合运动波（MMC）Ⅲ相活动，呈逆行传播或出现非传播性压力活动暴发群等，多数患者消化间期向消化期运动转换障碍。结论Roux肠袢运动紊乱，可能与患者术后发生Roux～Y综合征有关。     

Secrepan治疗慢性消化性溃疡和急性胃粘膜损害出血的疗效

作者评估持续静滴胰泌素制剂Secrepan对慢性消化性溃疡和急性胃粘膜损害(AGML)引起的胃十二指肠出血的止血作用。 37例患者,其中慢性消化性溃疡13例和AGML 24例。所有病人头3天接受Secrepan每小时2U/kg,后4天静滴每小时0.5 U/kg。结果慢性消化性溃疡患者经Secrepan     

小剂量一周奥美拉唑、替硝唑及克拉红霉素根除幽门螺杆菌和治愈消化性溃疡

大量文献表明，幽门螺杆菌可导致胃炎和胃及十二指肠溃疡。本文采用小剂量奥美拉华（omeprazole）、替硝唑（tinidazole）和克拉红霉素（darythromvcin）这种新型三联方案治疗消化性溃疡和根除幽门螺杆菌取得了令人满意的疗效。1方法116例患者经临床和活检证实伴有幽门螺杆菌的消化性溃疡患者进入本研究。其中活动性十二指肠溃疡35例、活动性胃溃疡6例、已愈合的十二指肠溃疡47例、类溃疡增生28例。所有病人均采用下列方案治疗一周。奥美拉唑20mg，每日2次2克拉红霉素25Omg，每日2次2替硝叹50Omg，每日2次。上述3种药物均于进餐时服用。中…     

非溃疡性消化不良儿童胃电图异常及西沙必利的临床疗效

应用体表胃电图对50例非溃疡性消化不良(NUD)儿童和20名正常儿童进行测试,结果显示:NUD儿童胃电主频减慢,节律紊乱和图型不规则,与正常儿童相比具有显著性差异(P＜0.01).提示NUD儿童胃动力不足,经服用促胃动力药西沙必利后,临床疗效显著.     

红霉素促进胃肠运动

1989年5月13～19日在美国华盛顿特区召开的美国胃肠学会第90次年会上有几篇关于红霉素对胃肠道运动影响的报道。近年来的研究证明红霉素是一种胃动素(Motilin)激动剂,在狗和人体证明红霉素能诱导三相最大运动收缩(MMC)活性并能与胃动素受体结合。胃动素的主要作用在胃十二指肠区,胃幽门窦和邻近十二指肠的肌条中胃动素受体密度最大,收缩作用也最强。Depoortere等发现在家兔模型中红霉素、Sandostatin(胃动素分泌抑制剂)都能对胃动素受体进行调节,红霉素导致高胃动素血症,Sandostatin引起低胃动素血症,因此红霉素被认为是前运动(prokinetical)药物。     

The effect of helicobacter pylori eradication therapy on gastric antral myoelectrical activity and gastric emptying in patients with non-ulcer dyspepsia

BACKGROUND: Dysmotility of the gastroduodenal region and delayed gastric emptying have been considered to play roles in non-ulcer dyspepsia. In addition, it has been reported that Helicobacter pylori induced inflammation of the gastric mucosa may affect gastric motility. AIM: To evaluate the effects of H. pylori eradication therapy on gastrointestinal motility and symptoms in non-ulcer dyspepsia patients. METHODS: A total of 46 non-ulcer dyspepsia patients were examined for gastric emptying, antral myoelectrical activity, H. pylori infection, and symptom scores. In H. pylori-positive non-ulcer dyspepsia patients, gastric emptying, antral myoelectrical activity, and symptom scores were also analysed 2 months after being cured of H. pylori infection. RESULTS: A total of 67.4% of the non-ulcer dyspepsia patients were H. pylori-positive. Both abnormal gastric emptying and antral myoelectrical activity were observed in non-ulcer dyspepsia patients. H. pylori-positive non-ulcer dyspepsia patients were divided into three groups according to their gastric emptying: the delayed gastric emptying group, the normal gastric emptying group, and the rapid gastric emptying group. In the delayed and rapid gastric emptying groups, the gastric emptying and symptom scores were improved significantly by the eradication therapy. However, there was no improvement in symptom scores in the normal gastric emptying non-ulcer dyspepsia group by the eradication therapy. CONCLUSIONS: Disturbed gastric emptying and antral myoelectrical activity play roles in non-ulcer dyspepsia. Helicobacter pylori infection, inducing disturbed gastric emptying, may cause some non-ulcer dyspepsia symptoms. Gastric emptying and symptom scores are improved by H. pylori eradication therapy in non-ulcer dyspepsia patients with disturbed gastric emptying. H. pylori eradication therapy is effective in H. pylori-positive non-ulcer dyspepsia patients with disturbed gastric emptying.     

Disturbed bowel habits in patients with non-ulcer dyspepsia

BACKGROUND; Emerging medications for non-ulcer-dyspepsia, such as the serotonin-receptor modulators, also affect bowel habits by altering colonic transit. If drugs that alter colonic function were to prove useful in non-ulcer dyspepsia, knowledge of baseline bowel habit disturbances would be potentially critical. AIM: To estimate the rate of non-ulcer dyspepsia patients with clinically relevant constipation or diarrhoea potentially precluding use of motility agents. METHODS: Consecutive patients with non-ulcer dyspepsia (n = 79), gastro-oesophageal reflux disease (n = 135) and organic upper gastrointestinal disease (upper gastrointestinal disease; n = 36) completed a validated symptom questionnaire evaluating predominant bowel habits in the last year. RESULTS: Prevalence of constipation was higher in non-ulcer dyspepsia (34%) than in gastro-oesophageal reflux disease (P = 0.01) and organic upper gastrointestinal disease (P = 0.01), prevalence of alternating diarrhoea/constipation (24%) and diarrhoea (22%) was similar, while prevalence of normal bowel habits was significantly less in non-ulcer dyspepsia (20%; P = 0.01 vs. gastro-oesophageal reflux disease and P < 0.01 vs. organic upper gastrointestinal disease). Constipation was particularly frequent in ulcer-like and dysmotility-like non-ulcer dyspepsia, while prevalence of diarrhoea was lowest in dysmotility-like non-ulcer dyspepsia. A normal bowel habit was equally uncommon in male (21%) and female non-ulcer dyspepsia patients (20%). CONCLUSIONS: Only one of five non-ulcer dyspepsia patients had normal bowel habits based on clinical symptoms; constipation is particularly prevalent. Patients with functional dyspepsia who are prescribed motility altering drugs should be evaluated by taking a thorough bowel habit history.     

The role of Helicobacter pylori infection in non-ulcer dyspepsia

It is currently unclear whether Helicobacter pylori ( H. pylori ) infection plays a role in patients who fulfil the criteria for non-ulcer dyspepsia. This paper reviews evidence for H. pylori -induced changes in gastric emptying, gastrointestinal motility, gastric acid secretion, and gastric perception in patients with non-ulcer dyspepsia. Problems in study design and execution of non-ulcer dyspepsia treatment trials are discussed. The results of non-ulcer dyspepsia treatment trials which have been performed in H. pylori -positive patients are reviewed. To date none of them has convincingly shown that cure of the H. pylori infection leads to a sustained improvement in symptoms.     

GM-611 (Chugai Pharmaceutical)

GM-611 is an erythromycin derivative that acts as an agonist at the motilin receptor. It is being developed by Chugai as a potential treatment for gastric motility disorder [169036], as well as reflux esophagitis, non-ulcer dyspepsia and diabetic gastroparesis [347963]. GM-611 is in phase II trials in the US for reflux esophagitis [322624], [347955], [399349]. GM-611 acts by a novel mechanism whereby it stimulates and promotes peristalsis in the stomach and other segments of the gastrointestinal tract [334994]. The drug was shown to produce a dose-dependent sustained depolarization of rabbit duodenal smooth muscle. Depolarization appeared to be associated with activation of monovalent cation-selective channels [273336]. In December 2000, Credit Suisse First Boston predicted that successful development of GM-611 could lead to sales over $500 million [400228].     

Standard treatment for Helicobacter pylori infection is suboptimal in non-ulcer dyspepsia compared with duodenal ulcer in Chinese

BACKGROUND: Recent studies suggest that the Helicobacter pylori eradication rate in patients with non-ulcer dyspepsia is lower when compared to patients with peptic ulcer diseases. AIM: The aim of this study was to study the efficacy of triple therapy for H. pylori infection in patients with duodenal ulcer vs. patients with non-ulcer dyspepsia. METHODS: A total of 582 Chinese patients with proven H. pylori infection were recruited to receive: omeprazole 20 mg, amoxicillin 1000 mg and clarithromycin 500 mg all given twice daily for 7 days (OCA regime). Endoscopy with rapid urease test, histology and culture were performed before treatment. Post-treatment H. pylori status was determined by (13)C-urea breath test. Metronidazole, clarithromycin and amoxicillin resistance was defined as minimum inhibitory concentration (MIC) of >8 microg/mL, >1 microg/mL and >1 microg/mL, respectively. RESULTS: A significantly higher (intention-to-treat/per-protocol) eradication rate was found in patients with duodenal ulcer than those with non-ulcer dyspepsia (91/94% vs. 84/88% respectively, P = 0.011 and P = 0.016). Clarithromycin resistance rate was higher in patients with non-ulcer dyspepsia than those with duodenal ulcer (14% vs. 6%, P = 0.015). Clarithromycin resistance (40% vs. 5%, P < 0.001, OR 12, 95% CI: 5.7-24.3) and the diagnosis of non-ulcer dyspepsia (91% vs. 84%, P = 0.011, OR 2.0, 95% CI: 1.2-3.3) significantly affected the success of H. pylori eradication. CONCLUSION: Clarithromycin resistance accounts for the significantly lower and suboptimal H. pylori eradication rate of OCA regimen in Chinese patients with non-ulcer dyspepsia compared to those with duodenal ulcer.     

Dose-dependent stimulation of gallbladder contraction by intravenous erythromycin in man

We have previously shown that a single oral dose of 500 nig erythromycin causes gallbladder contraction. The effect of intravenous erythromycin on antroduodenal motility is dose-dependent; < 3 mg/kg body weight stimulates propagated contractions in a fashion similar to motilin while doses > 7 mg/kg cause giant non-propagated antral contractions not seen with motilin. Using ultrasound, we have examined the effect of differing doses of intravenous erythromycin on gallbladder motility in man. Erythromycin (1 mg/kg) caused fasting gallbladder contraction to 52 % of basal gallbladder volume (P < 0.001), and increased gallbladder emptying following a liquid meal (maximal percentage emptied 75 ± 6.8% vs. 58 ± 9.0% following saline, P < 0.05). Erythromycin (7 mg/kg) however, had no effect on gallbladder fasting or post-prandial motor activity. We conclude that the effect of erythromycin on gallbladder motility is dose-dependent, with higher doses having no effect. It is possible that at higher doses erythromycin stimulates other receptors in addition to the motilin receptor, and that the combined effect is different to the stimulation of the motilin receptor alone.     

The role of milk and lactose intolerance in Ethiopian patients with non-ulcer dyspepsia: a case control study

Milk intolerance, lactose intolerance and non-ulcer dyspepsia are common among Ethiopians. This study, therefore, was designed to find out if milk intolerance associated with lactase deficiency account for non-ulcer dyspepsia. Ninety-eight patients with non-ulcer dyspepsia and 95 controls were examined and interviewed for demographic data and milk drinking habits. Then each had a lactose tolerance test (LTT), stool examination for pH, ova and parasites. The demographic characteristics and the number of milk drinkers were comparable in the 2 groups. However, milk intolerance and lactose intolerance were significantly higher among the patients with non-ulcer dyspepsia than among the control group (p less than 0.01, p less than 0.05 respectively). The combination of milk intolerance, lactose intolerance and LTT was also significantly different (p less than 0.01). The mean stool pH was markedly reduced after lactose ingestion and there were more ova and parasites in the stools of the control group. These observations suggest that milk intolerance and/or lactose intolerance account significantly for the symptoms of the patients with non-ulcer dyspepsia. However, since lactose intolerance and abnormal LTT are very common among adult Ethiopians symptoms related to the drinking of milk should be interpreted with caution vis-a-vis the results of the lactose loading test.     

A double‐blind placebo‐controlled study of buspirone‐stimulated prolactin release in non‐ulcer dyspepsia—are central serotoninergic responses enhanced?

BACKGROUND: Dyspepsia is a common symptom for which an organic cause is found in only 40% of patients. When no cause is apparent and the dyspepsia is considered to be idiopathic, a diagnosis of non-ulcer dyspepsia is made. The pathophysiology of non-ulcer dyspepsia is poorly understood and numerous theories have been put forward, including a theory of enhanced central serotoninergic receptor sensitivity. AIM: To determine the sensitivity of serotonin receptors in non-ulcer dyspepsia. METHODS: Using a randomized, double-blind, placebo-controlled design, we compared buspirone (a serotonin type 1a partial agonist)-stimulated prolactin release in 50 patients and 59 healthy comparison subjects. Buspirone, 30 mg, or matching placebo was administered on two separate occasions and prolactin release over 180 min was monitored. Patients and healthy subjects received both treatments in random order, 1 week apart. RESULTS: Overall, patients with non-ulcer dyspepsia had greater prolactin release in response to the buspirone challenge than the healthy comparison subjects, with differences most significant at 90 min following the challenge. Enhancement occurred in patients both with and without Helicobacter pylori infection. Female subjects, both patients and healthy volunteers, showed a greater response to buspirone than male subjects, and the augmentation of response observed in male and female patients was greater in females. CONCLUSIONS: Patients with non-ulcer dyspepsia have enhanced central serotoninergic responses and such responses are independent of H. pylori infection. Blockade of such receptors might be an appropriate therapeutic strategy.     

Optimal management of patients with non-ulcer dyspepsia: considerations for the treatment of the elderly.

Optimal therapy for patients with non-ulcer dyspepsia still remains elusive. Increasing consensus on the definition of non-ulcer dyspepsia may improve the design of clinical trials and result in more effective therapies for this common condition. This paper reviews the investigation, pathophysiology and therapy of non-ulcer dyspepsia in order to formulate management strategies in the elderly. The best outcome for the patient can be achieved by detailed evaluation, leading to therapy targeted to obvious precipitating factors such as dyspepsia-inducing medications and other aggravating factors such as slow-transit constipation. Prokinetics and, to a lesser extent, H(2) receptor antagonists are the main medications of choice. Cisapride, the best studied prokinetic, has been withdrawn from the market in certain countries because some patients experienced dangerous cardiac arrhythmias, especially when cisapride was given with potent inhibitors of cytochrome P450 3A4. Time spent on reassurance and judicious use of antidepressants for the right patient can help improve symptoms. In the elderly, however, persistent symptoms should be re-evaluated because of the increased incidence of malignancy.