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1.
24小时食管pH监测和食管测压在胃食管反流病中的应用 总被引:1,自引:0,他引:1
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。 相似文献
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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 … 总被引:7,自引:0,他引:7
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( 相似文献
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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。 相似文献
4.
血清,唾液铜锌超氧化物岐化酶测定在呼吸病中的应用 总被引:1,自引:0,他引:1
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)。 相似文献
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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 总被引:5,自引:0,他引:5
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。 相似文献
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7.
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 总被引:3,自引:1,他引:2
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。 相似文献
8.
食管测压对反流性食管炎的诊断价值 总被引:3,自引:2,他引:3
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(10±07对26±10;01±04对04±02,P均<001);食管中远段振幅(kPa)亦低于对照组(干咽:46±33对65±26,53±37对91±37,P均<005;湿咽:53±33对89±36,61±46对±124±45,P均<005).患者组LESL1(cm)比对照组短(17±08对26±09,P<001).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 相似文献
9.
一氧化氮在实验性反流性食管炎发病机制中的作用 总被引:11,自引:0,他引:11
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 相似文献
10.
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 总被引:5,自引:6,他引:5
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7998±3441和6364±2455.SASP组和NS组MDA含量(nmol/g)分别为2156±208、3524±448.NS组和SASP组炎症指数分别为165±519、630±125.SASP组SOD含量显著高于NS组(7998±3441对6364±2455,P<001),SASP组MDA含量明显低于NS组(2156±208对3524±448,P<001).NS组炎症指数明显高于SASP组(165±519对630±125,P<001).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. 相似文献
11.
肝硬化大鼠食管一氧化氮合酶分布定位研究 总被引:7,自引:2,他引:5
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。 相似文献
12.
[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。 相似文献
13.
Cheng P Gong J Wang T Jie C Liu GS Zhang R 《World journal of gastroenterology : WJG》2005,11(21):3277-3280
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. 相似文献
14.
Asaoka D Miwa H Hirai S Ohkawa A Kurosawa A Kawabe M Hojo M Nagahara A Minoo T Ohkura R Ohkusa T Sato N 《Journal of gastroenterology》2005,40(8):781-790
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. 相似文献
15.
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. 相似文献
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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 总被引:1,自引:0,他引:1
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。 相似文献
17.
Esophagitis in sprague-dawley rats is mediated by free radicals 总被引:10,自引:0,他引:10
Gerold J. Wetscher MD Galen Perdikis MD David H. Kretchmar PhD Ronald G. Stinson MD Debasis Bagchi PhD Elizabeth J. Redmond FRCS Thomas E. Adrian PhD Dr. Ronald A. Hinder MD PhD FACS 《Digestive diseases and sciences》1995,40(6):1297-1305
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. 相似文献
18.
兰索拉唑治疗反流性食管炎多中心临床观察 总被引:48,自引:0,他引:48
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。 相似文献
19.
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。 相似文献
20.
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 总被引:3,自引:1,他引:3
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。 相似文献