24小时食管pH监测和食管测压在胃食管反流病中的应用

目的：对８０例患者同时进行食管测压和２４小时ｐＨ值监测,探讨压力和２４小时ｐＨ值与胃食管反流及反流性食管 炎间的关系。方法：８０例病人分为Ａ组无反流症状;Ｂ组有反流症状,但内镜或Ｘ线检查无食管炎;Ｃ组有反流症状,内 镜或Ｘ线检查有食管炎。使用多导胃肠功能测定仪测定食管上、下括约肌及食管体静息和吞咽时压力及运动功能; 同时使用便携式２４小时ｐＨ监测仪监测食管２４小时ｐＨ值。结果：Ｂ、Ｃ两组的下食管括约肌压力（ＬＥＳＰ）低于Ａ组（Ｐ＜ ０．０５）,且食管下段蠕动幅度低于Ａ组（Ｐ＜０．０１）;Ｃ组食管下段蠕动低于Ｂ组（Ｐ＜０．０５）;２４小时ｐＨ监测Ｂ、Ｃ两组各项 指标均明显高于Ａ组（Ｐ＜０．００１）。结论：胃食管反流与ＬＥＳＰ降低、食管下段蠕动减弱有关,ＬＥＳＰ低于１１ｍｍＨｇ食管 炎的危险性增加。其诊断以２４小时ｐＨ监测结果为准。     

下食管括约肌压力与局部组织内一氧化氮和血管活性肠肽含量的 …

目的 研究下食管括约肌（ＬＥＳ）局部组织内一氧化氮（ＮＯ）和血管活性肠肽（ＶＩＰ）含量与ＬＥＳ压力（ＬＥＳＰ）的关系。方法 检测了１０８例食管运动功能障碍性疾病患者ＬＥＳ局部组织内ＮＯ和ＶＩＰ含量及ＬＥＳＰ。结果 ＬＥＳＰ与组织内ＮＯ和ＶＩＰ含量呈负相关（r＝－９０．７，Ｐ〈０．０１；r＝－９２．３，Ｐ〈０．０１），ＮＯ和ＶＩＰ含量之间呈正相关（r＝８８．５，Ｐ〈０．０１）。结论 胃食管反流性疾病（     

胃－食管返流的临床研究

作者采用国产ＳＧＹ－３型多功能消化道检测仪对８０例具有胃－食管返流（ＧＥＲ）症状患者进行了食管测压研究。患者分为两组：Ａ组３３例，内镜及活检食管粘膜正常；Ｂ组４７例，内镜及活检均证实有食管炎。正常对照组６０例。食管炎患者给予吗丁啉口服。结果显示：（１）Ａ、Ｂ两组患者食管下括约肌压力（ＬＥＳＰ）、胃－食管屏障压、食管下括约肌（ＬＥＳ）松驰率明显降低，ＬＥＳ松驰时间明显延长、ＬＥＳ长度（ＬＥＳＬ）短于正常，食管蠕动波压力明显降低（Ｐ＜０．０５，０．０１）；（２）Ｂ组ＬＥＳＰ、胃－食管屏障压明显低于Ａ组（Ｐ＜０．０５），这与临床上ＧＥＲ症状发生率Ｂ组高于Ａ组相符合；（３）吗丁啉使Ｂ组ＬＥＳＰ胃－食屏障压分别升高０．３９±０．４８和０．３４±０．４９ｋＰａ，但对食管蠕动无影响。因而，应用吗丁啉治疗ＬＥＳ功能低下引起的ＧＥＲ是合理、有效的。     

血清,唾液铜锌超氧化物岐化酶测定在呼吸病中的应用

作者测定了呼吸系疾病患者血清、唾液ＣｕＺｎ－ＳＯＤ含量，并与正常组对照比较，结果显示：重度肺结核血清ＣｕＺｎ－ＳＯＤ含量显著低于轻、中度患者（Ｐ＜０．０１），轻、中度肺结核治疗后ＣｕＺｎ－ＳＯＤ较治疗前明显降低（Ｐ＜０．０１）。肺癌组显著低于肺炎组（Ｐ＜０．０１）。     

卡托普利对缺血再灌注兔心肌一氧化氮及其合酶活性的影响

目的：探讨卡托普利（ｃａｐｔｏｐｒｉｌ）对局部缺血再灌注免心肌保护作用的机制。 方法：将１８只新西兰兔随机分３组（每组ｎ＝６）,对照组左冠状动脉前降支阻断３０分,再灌注９０分;卡托普利组阻断前３０分静脉注射卡托普利每 ２０分 ２ ｍｇ／ｋｇ,再灌注时再持续静脉注射卡托普利每 ９０分１ｍｇ／ｋｇ,假手术组环左冠状动脉前降支置线但不阻断血流。观察心肌一氧化氮合酶（ＮＯＳ）同工酶活性、过氧化物歧化酶活性、丙二醛含量、肌酸激酶含量及右心房血一氧化氮（ＮＯ）的变化,监测心肌功能。 结果：缺血再灌注心肌原生型ＮＯＳ（ＣＮＯＳ）活性（Ｐ＜０．００１）及总ＮＯＳ活性（Ｐ＜０．０１）显著下降,ＮＯ产生减少（Ｐ＜０．０５～０．０１）,卡托普利组缺血再灌注期间ＮＯ水平高于对照组（Ｐ＜０．０１）,再灌注３０分心肌ＣＮＯＳ活性（Ｐ＜０．０１）及总ＮＯＳ活性（Ｐ＜０．０５）显著高于对照组,心肌损害较对照组减轻。 结论：ＮＯ产生不足是心肌再灌注损伤的重要因素,卡托普利通过调节ＮＯＳ活性,维持正常ＮＯ水平起到保护作用。     

不同年龄大鼠组织NO含量和NOS活性的变化与衰老之间的关系

目的探讨组织一氧化氮（ＮＯ）含量与一氧化氮合酶（ＮＯＳ）活性的变化规律,揭示其与衰老的关系。方法采用铜离子活化镉还原法、硫代巴比妥酸染色法和血红蛋白氧化测定组织ＮＯ、丙二醛（ＭＤＡ）含量和ＮＯＳ的活性。结果与青年鼠组（４－５月龄相比,老年鼠组（２０－２２月龄）心脑肾组织ＮＯ降低差异显著性（Ｐ〈０．０１）,而中年鼠组（９－１０月龄）仅肾组织ＮＯ含量降低有显著性差异（Ｐ〈０．０５）。中年鼠组比较,老年     

急性心肌梗塞患者红细胞左旋精氨酸-一氧化氮途径的变化

目的：探讨急性心肌梗塞患者红细胞在旋精氨酸—一氧化氮（Ｌ－Ａｒｇ－ＮＯ）途径变化及临床意义。 方法：１４例急性心肌梗塞患者为急性心肌梗塞组,１０例健康成人为正常对照组,取静脉抗凝血,分离并提纯红细胞,同位素标记法测定~３Ｈ标记左旋精氨酸（~３Ｈ－Ｌ－Ａｒｇ）的转运动力学;分离统化一氧化氮合酶（ＮＯＳ）后测定其含量及活性,放射免疫法测定红细胞环磷酸鸟苷（ｃＧＭＰ）含量。 结果：急性心肌梗塞组患者红细胞①Ｌ－Ａｒｇ的总转运及Ｙ~＋载体的最大转运速率（Ｖｍａｘ）分别较正常对照组降低１４％（Ｐ＜０．０５）及 １８％（Ｐ＜０．０１）,米氏常数（Ｋｍ）分别增加３２％及 ４６％（Ｐ＜０．０１）;Ｙ＋Ｌ载体无改变。②ＮＯＳ含量及活性分别较正常对照组降低１３％（Ｐ＜０．０５）及４４％（Ｐ＜０．０１）。③ＣＧＭＰ含量较正常对照组下降２７％（Ｐ＜０．０５）。 结论：急性心肌梗塞患者红细胞Ｌ－Ａｒｇ－ＮＯ途径存在多环节功能障碍,导致一氧化氮（ＮＯ）生成减少,可能会促进急性心肌梗塞的进展。     

食管测压对反流性食管炎的诊断价值

目的探讨食管测压对反流性食管炎的诊断价值．方法使用专用软件控制的高分辨多道灌注测压系统（ＰＣｐｏｌｙｇｒａｆＨＲ瑞典产）测定了正常人１２例及反流性食管炎患者３２例的食管下括约肌动力指标、胸腹段长度及食管体动力参数．结果患者组ＬＥＳＰ，ＬＥＳＲＰ压力（ｋＰａ）明显低于对照组（１０±０７对２６±１０；０１±０４对０４±０２，Ｐ均＜００１）；食管中远段振幅（ｋＰａ）亦低于对照组（干咽：４６±３３对６５±２６，５３±３７对９１±３７，Ｐ均＜００５；湿咽：５３±３３对８９±３６，６１±４６对±１２４±４５，Ｐ均＜００５）．患者组ＬＥＳＬ１（ｃｍ）比对照组短（１７±０８对２６±０９，Ｐ＜００１）．结论反流性食管炎患者ＬＥＳＰ低下，ＬＳＥＬ１过短，食管体中远段动力低下，为临床选用动力药提供了客观依据     

一氧化氮在实验性反流性食管炎发病机制中的作用

目的　探讨一氧化氮(NO)在实验性反流性食管炎发病中的作用。方法　48 只SD大鼠随机分为3 组:A组:采用完全幽门结扎 贲门肌切开术;B组:采用半幽门缝扎 贲门肌切开术,分别制备反流性食管炎动物模型;C组:假手术对照组。并于模型制备后24小时、48 小时、72 小时观察食管下端粘膜的病理表现,测定食管组织的NO含量。结果　食管炎指数(肉眼和显微镜下),A 组术后24小时以及B组术后24 小时、48 小时、72 小时与C组比较差异均有非常显著意义( P< 0.01 );食管组织NO含量,A 组术后24小时以及B组术后24小时、48小时、72小时与C组比较,差异亦均有显著性意义(P< 0.05, P< 0.01 );不同程度食管炎组的食管组织NO 含量均明显高于非食管炎组(P<0.05,P< 0.01 ),而不同程度食管炎组间的食管组织NO含量差异无显著性意义(P> 0.05 )。结论　NO在实验性反流性食管炎发病机制中对食管粘膜可能发挥损伤和保护的双重作用     

柳氮磺胺吡啶对大鼠乙酸性溃疡性结肠炎肠组织中氧自由基的影响

目的探讨柳氮磺胺吡啶（ＳＡＳＰ）治疗大鼠乙酸性溃疡性结肠炎（ＵＣ）时清除氧自由基（ＯＦＲ）的特性．方法ＳＡＳＰ灌胃治疗大鼠乙酸性ＵＣ后，检测肠组织中的超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）含量，评价其炎症指数，并与生理盐水（ＮＳ）治疗对照组比较．结果ＳＡＳＰ组和ＮＳ组ＳＯＤ含量（Ｕ／ｇ）分别为７９９８±３４４１和６３６４±２４５５．ＳＡＳＰ组和ＮＳ组ＭＤＡ含量（ｎｍｏｌ／ｇ）分别为２１５６±２０８、３５２４±４４８．ＮＳ组和ＳＡＳＰ组炎症指数分别为１６５±５１９、６３０±１２５．ＳＡＳＰ组ＳＯＤ含量显著高于ＮＳ组（７９９８±３４４１对６３６４±２４５５，Ｐ＜００１），ＳＡＳＰ组ＭＤＡ含量明显低于ＮＳ组（２１５６±２０８对３５２４±４４８，Ｐ＜００１）．ＮＳ组炎症指数明显高于ＳＡＳＰ组（１６５±５１９对６３０±１２５，Ｐ＜００１）．结论ＳＡＳＰ为氧自由基清除剂，是治疗溃疡性结肠炎的主要机理之一．     

肝硬化大鼠食管一氧化氮合酶分布定位研究

目的探讨一氧化氮（ＮＯ）在肝硬化食管静脉曲张及血流动力学改变中的作用。方法应用还原型辅酶Ⅱ－黄递酶（ＮＡＤＰＨ－ｄ）组化染色观察ＣＣＩ４所致肝硬化大鼠食管下段一氧化氮合酶（ＮＯＳ）分布；应用荧光法检测大鼠食管组织匀浆及血清中ＮＯ含量；应用５７Ｃｏ标记微球测定大鼠血流动力学指标。结果肝硬化鼠食管粘膜及粘膜下血管内皮ＮＯＳ呈强阳性反应，而正常鼠则呈弱阳性或阴性反应；肝硬化大鼠食管及血清中ＮＯ含量显著升高。且全部出现门脉高压和高动力循环状态。结论ＮＯ在肝硬化大鼠食管静脉曲张及血流动力学改变中可能起重要作用。     

调中颗粒对混合反流性食管炎大鼠食管黏膜3种胃肠激素的影响

[目的]观察调中颗粒对混合反流性食管炎(RE)模型大鼠食管黏膜促胃液素(GAS)、一氧化氮合酶(NOS)和血管活性肠肽(VIP)3种胃肠激素的影响。[方法]通过食管、十二指肠端侧吻合术制备混合RE大鼠模型,随机分为调中颗粒组、半夏泻心汤组、西沙必利组、模型组、正常组,1周后同时分别给予调中颗粒、半夏泻心汤、西沙必利和0.85%氯化钠,连续给药14d后,观察食管黏膜GAS、NOS和VIP的水平。[结果]混合RE模型大鼠食管黏膜GAS水平显著降低,而NOS和VIP显著升高;用调中颗粒治疗后食管黏膜GAS水平升高,而NOS与VIP显著降低,与正常组相比差异无统计学意义(P>0.05)。[结论]调中颗粒通过调节食管黏膜GAS、NOS和VIP水平治疗混合RE。     

Gene expression in Barrett＇s esophagus and reflux esophagitis induced by gastroduodenoesophageal reflux in rats

AIM: To investigate the difference of gene expression profiles between Barrett's esophagus and reflux esophagitis induced by gastroduodenoesophageal reflux in rats. METHODS: Eight-week-old Sprague-Dawley rats were treated esophagoduodenostomy to produce gastroduodenoesophageal reflux, and another group received sham operation as control. Esophageal epithelial tissues were dissected and frozen in liquid nitrogen immediately for pathology 40 wk after surgery. The expression profiles of 4 096 genes in reflux esophagitis and Barrett's esophagus tissues were compared with normal esophageal epithelium by cDNA microarray. RESULTS: Four hundred and forty-eight genes in Barrett's esophagus were more than three times different from those in normal esophageal epithelium, including 312 up-regulated and 136 down-regulated genes. Two hundred and thirty-two genes in RE were more than three times different from those in normal esophageal epithelium, 90 up-regulated and 142 down-regulated genes. Compared to reflux esophagitis, there were 214 up-regulated and 142 down-regulated genes in Barrett's esophagus. CONCLUSION: Esophageal epithelium exposed excessively to harmful ingredients of duodenal and gastric reflux can develop esophagitis and Barrett's esophagus gradually. The gene expression level is different between reflux esophagitis and Barrett's esophagus and the differentially expressed genes might be related to the occurrence and development of Barrett's esophagus and the promotion or progression in adenocarcinoma.     

Altered localization and expression of tight-junction proteins in a rat model with chronic acid reflux esophagitis

Background The esophageal tight junction is responsible for the paracellular sealing of the epithelium. Alteration of the expression of tight-junction proteins plays crucial roles in the pathogenesis of some human diseases. The aim of this study was to investigate the distribution and expression pattern of tight-junction proteins in the esophageal mucosa of control rats and rats with reflux esophagitis.Methods Chronic acid reflux esophagitis was experimentally induced by operation in rats. The animals were killed on days 7 and 14 after the operation. The thickness of the mucosa and the 5-bromo-2-deoxyuridine (BrdU) labeling index were assessed. The expression pattern of the tight-junction proteins claudin 1-4 and occludin in the esophageal mucosa was investigated by immunofluorescence staining and Western blotting in the controls and esophagitis rats.Results In the esophagitis model, the thickness and BrdU labeling index increased with time. In control rats, claudin-1, -3, and -4 were localized on the cellular membranes of esophageal epithelial cells, mainly in the spinous and granular layers, while claudin-2 was not detected in any layer. Occludin was seen on the cellular membranes in all esophageal mucosal layers. In the esophagitis rats, the expression of claudin-1 was increased both in the plasma membrane and in the cytoplasm around the erosion in the spinous and granular layers. The expression of claudin-4 and occludin shifted to the cytoplasm from the plasma membrane in the spinous and granular layers. In contrast, the expression of claudin-3 was decreased in the spinous and granular layers.Conclusions The localization and the expression patterns of tight-junction proteins were different in the controls and the rat esophagitis model. The expression of claudin-3 in the esophageal mucosa was decreased, while that of claudin-1 was increased. It is postulated that these alterations in tight-junction proteins most likely increase the permeability of the esophageal the epithelium, thereby impairing the defense mechanism of this epithelium.     

Physiological studies on nitric oxide in the lower esophageal sphincter of patients with reflux esophagitis

BACKGROUND/AIMS: Nitric oxide has recently been shown to be a neurotransmitter in the non-adrenergic non-cholinergic inhibitory nerves in the digestive tract. To clarify the significance of nitric oxide in the lower esophageal sphincter of patients with reflux esophagitis, we have investigated enteric nerve responses in lower esophageal sphincter specimens obtained from the patients with gastric cancer who had reflux esophagitis, using the normal lower esophageal sphincter as a control. METHODOLOGY: Lower esophageal sphincter specimens were obtained from 6 patients who had gastric cancer with reflux esophagitis, and normal lower esophageal sphincter specimens were obtained from 12 patients who had gastric cancer without gastroesophageal reflux disease. A mechanograph was used to evaluate in vitro lower esophageal sphincter muscle responses to electrical field stimulation of the adrenergic and cholinergic nerves before and after treatment with various autonomic nerve blockers, and NG-nitro-L-arginine and L-arginine. RESULTS: 1) Cholinergic nerves were more dominant in the normal lower esophageal sphincter than in the lower esophageal sphincter with reflux esophagitis (p < 0.01); 2) non-adrenergic non-cholinergic inhibitory nerves were significantly found to act more on the lower esophageal sphincter with reflux esophagitis than those in the normal lower esophageal sphincter (p < 0.01); 3) nitric oxide mediates the relaxation reaction via non-adrenergic non-cholinergic inhibitory nerves in the normal lower esophageal sphincter and the lower esophageal sphincter with reflux esophagitis; 4) The relaxation reaction of nitric oxide was observed in the normal lower esophageal sphincter and increased in the lower esophageal sphincter with reflux esophagitis. CONCLUSIONS: These findings suggest that the cholinergic and non-adrenergic non-cholinergic inhibitory nerves play important roles in regulating contraction and relaxation of the human lower esophageal sphincter, and nitric oxide plays an important role in non-adrenergic non-cholinergic inhibitory nerves of the human lower esophageal sphincter. In addition, a decrease of the action of cholinergic nerves and an increase of the action of non-adrenergic non-cholinergic inhibitory nerves by nitric oxide may be largely related to the low lower esophageal sphincter pressure observed in the patients with reflux esophagitis.     

左旋哨基精氨酸甲基酯对大鼠食管静脉曲张影响的酶组化研究

目的：探讨一氧化氮（NO）在食管静脉曲张发生机制中的作用,初步观察使用一氧化氮合酶（NOS）抑制剂治疗食管静脉曲张的可能性。方法：采用NADPH－d黄递酶组化染色与图像分析方法,观察NOS抑制剂左旋肖基精氨酸甲基酯（L－NAME）灌胃给药对食管静脉曲张大鼠食管壁组织学改变及NOS表达平均光密度值的影响。结果：模型组食管、粘膜下静脉壁及食管浆膜外静脉壁粘膜上皮NOS表达较假手术组增多,给予L－NAME后,食管壁NOS表达显著下调（P＜0．01）,L－NAME组10只大鼠中7只食管浆膜外静脉和粘膜下静脉迂曲扩张情况较模型组减轻。结论;大鼠食管静脉曲张的发病机制中有NO的参与;L－NAME对大鼠食管静脉曲张具有一定保护作用。     

Esophagitis in sprague-dawley rats is mediated by free radicals

Free radical-mediated esophagitis was studied during duodenogastroesophageal reflux (mixed reflux) or acid reflux in rats. The influence of reflux on esophageal glutathione levels was also examined. Mixed reflux caused more gross mucosal injury than acid reflux. Gross mucosal injury occurred in the mid-esophagus. Total glutathione (GSH) in the esophageal mucosa of control rats was highest in the distal esophagus. The time course of esophageal GSH in rats treated by mixed reflux showed a significant decrease 4 hr after initiation of reflux, followed by a significant increase from the 12th hour on. Mucosal GSH was increased in both reflux groups after 24 hr but significantly more so in the mixed than in the acid reflux group. The free radical scavenger superoxide dismutase (SOD) prevented esophagitis and was associated with decreased GSH levels. GSH depletion by buthionine sulfoximine (BSO) prevented esophagitis and stimulated SOD production in the esophageal mucosa. It is concluded that gastroesophageal reflux is associated with oxidative stress in the esophageal mucosa. The lower GSH levels in the mid-esophagus may predispose to damage in this area. Duodenogastroesophageal reflux causes more damage than pure acid reflux. Oxidative stress leads to GSH depletion of the esophageal mucosa in the first few hours following damage but then stimulates GSH production. GSH depletion by BSO does not worsen esophagitis since it increases the esophageal SOD concentration.     

Ki-67在Barrett食管、重度反流性食管炎和食管腺癌中的表达和意义

背景：Barrett食管是一种食管腺癌癌前病变。Ki-67是一种能较准确地评估细胞增殖状态的抗原，在肿瘤进程中可能起重要作用。目的：研究Ki-67在Barrett食管、重度反流性食管炎和食管腺癌中的表达和意义。方法：应用免疫组化SP法测定59例Barrett食管、5例重度反流性食管炎、5例食管腺癌和10例正常食管黏膜组织中Ki-67的表达。结果：Ki-67在重度反流性食管炎中的阳性率为80．0％，Barrett食管阳性率为76．3％，与正常食管黏膜组织（20．0％）相比有显著差异（P〈0．05）：食管腺癌阳性率为100％。Ki-67的表达随Barrett食管肠化生程度的加重而增高（P〈0．05）；而不同长度（短段、长段）、肠化生黏膜形态（全周型、舌型和岛型）以及不同程度（轻度、中度）异型增生的Barrett食管，Ki-67的表达均无显著差异（P〉0．05）。结论：Ki-67在重度反流性食管炎和Barrett食管中表达增强，提示其在食管腺癌进程中起重要作用。     

环氧合酶-2在反流性食管炎大鼠食管组织中表达的实验研究

背景：环氧合酶（COX）-2在炎症、肿瘤等的发生、发展过程中发挥重要作用，但其在反流性食管炎（RE）中的作用尚未明确。目的：研究COX-2在混合性RE大鼠食管组织中的表达，探讨COX-2的表达与RE的关系。方法：采用贲门肌切开术加十二指肠半结扎术建立混合性RE大鼠模型。22只健康Sprague-Dawley大鼠随机分为RE模型组（n=12）和假手术组（n=10），于术前和术后1周测定食管下段和胃液pH值。处死大鼠，分别应用放射免疫测定和免疫组化方法检测食管组织中前列腺素（PG）E2的含量和COX-2的表达，光镜观察食管组织的形态学改变。结果：RE模型组术后食管下段pH值显著低于假手术组（P〈0．05），胃液pH值则显著高于假手术组（P〈0．05）；食管组织PGE2含量亦较假手术组显著增高（P〈0．001），COX-2表达均为阳性，假手术组食管组织中无COX-2表达。光镜观察显示RE模型组食管黏膜病理损害明显。结论：COX-2高表达和PGE2含量增高参与了混合性RE的发生、发展过程，COX-2可能通过升高PGE2含量而在RE的发病中起重要作用。     

兰索拉唑治疗反流性食管炎多中心临床观察

目的探讨兰索拉唑对反流性食管炎的疗效。方法上海地区４所医院用兰索拉唑３０ｍｇ,每日一次,治疗９２例经内镜证实的反流性食管炎患者。分别于治疗后２、４、６周观察反酸、烧心、反食等症状疗效,并于６周后复查胃镜,观察镜下治愈率,其中１０例患者分别与治疗前、后进行食管２４小时ｐＨ监测。结果兰索拉唑治疗２周,即可见症状明显改善,症状记分较治疗前明显下降（Ｐ＜０．０１）,治疗２、４、６周后,症状治疗显效率分别为５３．２６％、８０．４３％及８２．６１％（治疗４周及６周后,与２周比,Ｐ＜０．０１）。治疗６周症状改善总有效率为９３．４８％。６周后Ⅰ级食管炎治愈率为９３．７５％,高于Ⅱ级７５．７６％、Ⅲ级与Ⅳ级６３．６４％（Ｐ＜０．０５）;但各级食管炎改善,即有效率比较差异无显著性。１０例进行食管２４小时ｐＨ监测患者,治疗后,反流总时间百分率及反流总次数分别由１６．３７±５．９３％及１５０．２±３６．５０次,降至４．８１±０．４４％（Ｐ＜０．０１）及５８．１±１６．９９次（Ｐ＜０．０１）。结论兰索拉唑是治疗反流性食管炎的有效药物。