内皮素在大鼠冷束缚应激性溃疡中的作用

本研究采用大鼠冷束缚应激溃疡模型,动态检测了应激前及应激后血浆、胃粘膜组织内皮素-1(ET-1)含量、胃粘膜血流量(GMBF)及溃疡指数(UI)的变化,及内皮素转化酶抑制剂phosphora-midon对应激性溃疡时GMBF、UI的影响,旨在探讨内源性ET-1在应激性溃疡发生中的可能作用机     

老年消化性溃疡的治疗

老年消化性溃疡的定义及特点从40岁开始胃液(包括胃酸和胃蛋白酶)的分泌便减少,胃粘膜血流量也降低,同时发生明显的萎缩性胃炎及胃粘膜肠上皮化生。由于抗溃疡因素降低而引起的粘膜损害及溃疡形成,发生于65岁以上时,便可称为老年消化性溃疡。老年消化性溃疡中胃溃疡多于十二指肠溃疡,日本为3∶1。老年胃溃疡有以下特点:它往往表现为     

胃粘膜血流变化的影响因素

维持和增加胃粘膜血流(gastric mucosal blood flow,GMBF)被认为是增加胃粘膜保护机制的关键因素,对GMBF影响因素的研究为临床防治消化性溃疡、慢性胃炎、胃癌等疾病提供了依据。影响GMBF的因素很多,现综述如下。 1 神经因素中枢神经系统中主要是下丘脑和延髓对GMBF有影响,下丘脑对GMBF的影响可能是由去甲肾上腺素介导的。交感神经节后纤维分布于胃血管壁周围,主要通过释放去甲肾上腺素使胃粘膜血管收缩,使GMBF减少。α受体拮抗剂能减少电刺激交感神经或动脉灌注儿茶酚胺所引起的GMBF减少,电刺激迷走神经,其节前纤维主要释放乙酰胆碱增加,致     

一氧化氮,内皮素与胃粘膜损伤

胃粘膜损伤是内源性扩血管因子和缩血管因子失衡 ,胃粘膜血流 (GMBF)减少所致。一氧化氮 (NO)和内皮素 (ET)是体内一对相互拮抗的血管活性物质。内源性NO/ET失衡 ,可致GMBF减少 ,导致胃粘膜损伤。     

消化性溃疡和慢性胃炎患者粘膜病变的特点分析

目的观察消化性溃疡和慢性胃炎患者胃粘膜病变特点．方法十二指肠溃疡80例，胃溃疡93例，肾十二指肠复合溃疡72例，慢性胃炎254例，均由内镜证实．取病变处，胃窦大弯，胃体小弯部胃粘膜活检．常规石腊包埋切片，HE染色，按全国统一标准诊断统计学处理采用u检验结果各组粘膜炎症发生率均高于萎缩和其他病变发生率．胃溃疡萎缩发生率高，肠上皮化生及非典型增生亦较多．十二指肠溃疡萎缩发生率最低．随年龄增高，消化性溃疡胃粘膜萎缩发生率增加．女性患者胃粘膜发生萎缩者较多．十二指肠溃疡以单纯慢性炎症为主，炎症及萎缩程度轻．而其他组则以慢性活动炎症为主，以胃溃疡较为严重结论本组资料提示胃溃疡与胃炎的发病关系密切，而胃溃疡产生胃粘膜萎缩亦较为常见十二指肠溃疡患者胃粘膜病变轻微且局限．萎缩发生少．     

内镜下胃粘膜血流测定和硬化治疗对肝硬化患者的影响

急诊内镜检查表明,除食管静脉曲张破裂外,出血性胃炎或急性胃粘膜病变亦为肝硬化患者呕血的原因。作者用非分流手术(食管横断+脾切除)或内镜下硬化剂治疗食管静脉出血,但术后有时不仅遇到曲张静脉再出血的病例,且有出血性胃粘膜病变病例。为了评估食管横断和硬化治疗对胃粘膜血流(GMBF)的影响,作     

血管活性肠肽参与电针对大鼠胃粘膜损伤的保护作用

目的：探讨血管活性肠肽(VIP)参与电针对胃粘膜损伤大鼠保护作用的机制。方法：采用束缚冷应激胃粘膜损伤大鼠模型，通过放射免疫测定法和中枢迷走背核复合体(DVC)微量注射，观察电针对各组外周血、胃粘膜和脑组织的VIP含量的变化，胃粘膜血流量(GMBF)、损伤指数(LI)和跨壁电位差(PD)的影响。结果：电针模型组外周血、胃粘膜和脑组织VIP含量均增加，GMBF、PD也明显增加，LI下降；中枢DVC微量注射VIP后，外周血和胃粘膜中VIP含量增加。结论：VIP作为信号分子，通过神经内分泌免疫网络系统对胃粘膜损伤具有整体调控作用。     

根除幽门螺杆菌对胃溃疡粘膜局部氧化应激反应的影响

目的：研究幽门螺杆菌(H．pylori)阳性胃溃疡患根除H．pylori前后胃粘膜局部氧化应激反应的改变。方法：对72例H．pylori阳性胃溃疡患三联杀菌治疗前后的溃疡边缘粘膜组织行活性氧(ROS)、白细胞介素8(1L-8)含量及炎症积分测定。结果：在H．pyLori根除后，胃粘膜ROS、IL-8含量及炎症积分均较根除前明显下降(P＜0．00l及P＜0．01)。结论：根除H．pylori可抑制致炎因子IL-8表达及减少ROS生成，从而降低胃溃疡粘膜局部氧化应激反应，减轻粘膜炎症，利于溃疡愈合。     

内皮素、一氧化氮在内毒素血症大鼠胃粘膜损伤中的作用

目的研究ET-1/NO)失衡在内毒素血症胃粘膜损伤中的作用.方法实验选用Wistar大鼠30只,随机分成5组,每组6只,于0,20min腹腔分别注射如下两组药物.正常组:生理盐水+生理盐水.内毒素(LPS)组:LPS+生理盐水.特异性内皮素受体(ETAR)阻滞剂BQ-123组:LPS+BQ-123.NO前体L-精氨酸(L-Arg)组:LPS+L-Arg.一氧化氮合酶阻滞剂NG-硝基-L-精氨酸甲酯(L-NAME)组:LPS+L-NAME.于60min分别测定血浆、胃粘膜中ET-1,NO含量变化,以及胃粘膜血流(GMBF)、胃粘膜损伤面积的变化.结果 LPS组ET-1水平较正常组显著增高(P<0.05),NO,GMBF较正常组显著减少(P<0.05),溃疡指数显著增加(P<0.05).而BQ-123组GMBF较LPS组显著改善(P<0.05),溃疡指数显著降低(P<0.05).L-Arg组NO,GMBF较LPS组显著升高(P<0.05),ET-1水平则较LPS组显著降低(P<0.05),溃疡指数显著降低(P<0.05).L-NAME组NO,GMBF较LPS组显著减少(P<0.05),溃疡指数显著增加(P<0.05).结论内源性ET-1/NO失衡参与了内毒素血症时胃粘膜损伤病理过程.纠正内源性ET-1/NO失衡,通过改善胃粘膜血流(GMBF),减轻胃粘膜损伤.     

幽门螺杆菌Cag A抗体的临床意义

对慢性胃炎、消化性溃疡患者进行细胞毒素相关基因蛋白 (ＣａｇＡ)抗体检测 ,并测定血清幽门螺杆菌 (Ｈｐ)抗体ＩｇＧ浓度 ,以探索血清ＣａｇＡ ＨｐＩｇＧ与十二指肠球部溃疡 (ＤＵ)、胃溃疡、慢性胃炎的关系 ,为临床诊治Ｈｐ感染提供参考。一、对象与方法1 病例资料 :我院门诊或住院病人 110例 ,男 48例、女6 2例 ,年龄 2 3～ 83岁 ,经胃镜证实为ＤＵ 30例、胃溃疡 15例、慢性胃炎 6 5例且同时抽取静脉血进行抗ＣａｇＡ ＨｐＩｇＧ和ＨｐＩｇＧ的检测。此外 ,选择男 15例、女 2 5例 ,共 40例健康、仅轻微或无消化道症状者作为对照组也进行…     

应激状态下大鼠胃黏膜组织中内皮素-1A受体mRNA的表达及其意义

应激性溃疡(SU)是危重疾病的常见严重并发症,其发生机制尚不清楚。研究表明内源性缩血管因子内皮素(ET)-1与SU密切相关,而关于其受体表达在SU发生中作用的研究尚少。目的:探讨ET-1A受体(ETAR)mRNA表达在SU发生中的作用和意义。方法:以冷束缚应激(CRS)制备大鼠胃溃疡模型,应激前和应激1 h、3 h、6 h、9 h、12 h后分别采用放射免疫测定、逆转录聚合酶链反应(RT-PCR)和斑点杂交等方法,动态检测血浆和胃黏膜组织中的ET-1和胃黏膜组织中的ETAR mRNA水平,同时检测胃黏膜血流量(GMBF)和溃疡指数(UI)等指标的变化情况。结果:与正常对照组相比,各应激组大鼠血浆和胃黏膜组织中的ET-1水平均显著升高(P<0.05),GMBF显著下降(P<0.01),UI显著增加(P<0.01);胃黏膜组织中的ET-1水平与UI呈显著正相关(r=0.98,P<0.01),与GMBF呈显著负相关(r=-0.89,P<0.05),而血浆ET-1水平与GMBF、UI相关性不显著(r=-0.61,0.43,P>0.05)。GMBF与UI呈显著负相关(r=-0.98,P<0.01)。RT-PCR和斑点杂交显示各应激组大鼠胃黏膜组织中ETAR mRNA的表达水平较正常对照组显著升高(P<0.01),并与胃黏膜组织中的ET-1水平和UI呈显著正相关(r=0.93,0.95,P<0.01)。结论:在CRS诱发大鼠急性胃黏膜损伤的过程中,胃黏膜组织可显著增加ET-1的合成分泌和ETAR mRNA的     

Preventive Effects of Rebamipide on NSAID-Induced Gastric Mucosal Injury and Reduction of Gastric Mucosal Blood Flow in Healthy Volunteers

The precise mechanisms of acute damage and the role of gastric mucosal blood flow in gastric mucosal injury induced by nonsteroidal anti-inflammatory drugs (NSAIDs) remain uncertain. The aim of this study was to evaluate the preventive effect of rebamipide on gastric mucosal injury and reduction of gastric mucosal blood flow (GMBF) after ibuprofen administration. Twenty healthy volunteers were randomized two groups. The rebamipide group took ibuprofen, 1800 mg/day, and rebamipide, 100 mg t.i.d., for 7 days. The placebo group took ibuprofen, 1800 mg/day. The numbers of gastric ulcer subjects were three in the placebo group and zero in the rebamipide group. The mean modified Lanza score after ibuprofen administration was significantly higher in the placebo group than the rebamipide group (2.9±1.7 vs. 1.3±1.0, respectively; P=0.032). The GMBF of the placebo group was significantly decreased at antrum from baseline, from 2.8±0.5 to 2.0±0.5 tissue perfusion units (P=0.005). There was no difference in GMBF change in the rebamipide group. Gastric mucosal injury was correlated with GMBF reduction in antrum (r=−0.677, P=0.001). In conclusion, it is suggested that the decrease in GMBF may have been associated with NSAID-induced gastric mucosal injury, and rebamipide may have prevented NSIAD-induced gastric mucosal injury by maintaining GMBF in healthy subjects.     

不同饮食对大鼠十二指肠溃疡愈合的影响及胃粘膜的保护作用

目的:观察小米。大米。面粉和全脂奶饮食对实验性十二指肠溃疡(DU愈合的影响及胃粘膜的保护作用,寻求DU患者更为合理的饮食种类。方法:应用5%半胱胺盐酸盐建立实验性大鼠DU模型,给予不同饮食后测定胃粘膜电位差(PD。前列腺素E2(PGE2)含量。计算溃疡指数(UI)及判定溃疡愈合程度。结果:小米组和大米组的UI分别为2.60±1.71和3.00±1.77,低于面粉组4.70±1.77(P<0.05);全脂奶组UI与以上三组相比无显著差异(P>0.05)。胃粘膜组织中PGE2含量亦以小米组和大米组为高,分别为1802.40 pg/mg±567.26pg/mg和1706.86pg/mg±429.08 pg/mg,与面粉组和全脂奶组相比差异显著(P<0.01,P<0.05)。胃粘膜PD检测:小米组为-22.32±10.59;面粉组为-11.76±8.08,两组相比差异显著(P<0.05)。结论:通过胃粘膜PD的检测,反映小米饮食可提高胃粘膜屏障的完整性;小米和大米饮食可增加胃粘膜组织中PGE2含量,对实验性大鼠DU愈合作用优于面粉饮食。     

左旋精氨酸甲酯及左旋精氨酸对应激状态下胃黏膜耐受性细胞保护作用的影响

目的：探讨内源性一氧化氮（NO）在应激状态下胃黏膜耐受性细胞保护中的作用及其可能的机制。方法：以重复浸水束缚应激（WRS）制作动物模型,以左旋精氨酸甲酯（L－NAME）或左旋精氨酸（L－Arg）抑制或促进内源性NO的合成,动态检测胃黏膜血流量（GMBF）、溃疡指数（UI）、黏膜一化氮含量的变化。结果：重复应激后,实验对照组大鼠UI明显下降,同时GMBF上升,黏膜内NO含量增高;L－NAME使WWRS引起的胃黏膜损伤加重,消除了GMBF的递增趋势,黏膜NO含量下降;而L－Arg可减轻WRS造成的黏膜损伤,GMBF、黏膜NO含量增相应增加;GMBF、UI、黏膜NO含量变化之间有相关关系。结论：内源性NO通过调节GMBF而介导耐受性细胞保护作用,L－NAME抑制其合成,延缓这一作用,L－Arg增加其合成,促进该作用。     

Gastric mucosal blood flow response to stress in streptozotocin diabetic rats: Regulatory role of nitric oxide

To investigate cytoprotection against mucosal injuries of the stomach in patients with diabetes, we investigated gastric mucosal blood flow (GMBF), its response to a burn stress, and the involvement of nitric oxide (NO) in streptozotocin (STZ) diabetic rats. GMBF was measured by laser-Doppler velocimetry (LDV) and by the hydrogen gas clearance technique (HGC). The steady-state GMBF of STZ rats decreased according to the duration of diabetes, and insulin treatment blocked this decrease. Burn stress caused a rapid decrease in the GMBF. Reduction of the GMBF and gastric mucosal leakage of Evans blue (EB) after the burn stress were greater in the STZ rats than in the controls, but insulin treatment completely blocked this increase in EB leakage in the STZ rats. There was a significant negative correlation between the percent GMBF 3 h after the burn stress and EB leakage at the same time point. In the controls and the insulin-treated STZ rats, N-nitro-l-arginine (l-NNA) an NO synthase inhibitor, enhanced the decrease in postburn GMBF and EB leakage, but was without effect in the STZ rats. These results suggest that NO may be involved in the regulation of GMBF, and that persistent hyperglycemia may impair this regulation. These findings suggest that patients with diabetes have reduced cytoprotection against a variety of gastric mucosal injuries.     

Mucosal irritative and healing impairment action of risedronate in rat stomachs: comparison with alendronate

BACKGROUND AND AIM: We used alendronate and risedronate as bisphosphonates and examined whether or not these agents have a mucosal irritative action in the stomach and impair the healing of pre-existing gastric ulcers in rats. METHODS: Male Sprague Dawley (SD) rats were used in the following two studies: (i) the effects of risedronate and alendronate on gastric potential difference (PD), gastric mucosal blood flow (GMBF) and acid back-diffusion in the stomach mounted on ex vivo chamber under urethane anesthesia and; (ii) the influence of daily treatment with these drugs on the healing of acetic acid-induced gastric ulcers was examined. RESULTS: Mucosal application of risedronate produced PD reduction in the saline-perfused stomachs in a dose-dependent manner. Alendronate also produced a marked PD reduction, the effect being more potent than that of risedronate. In the stomach exposed to acid (100 mM HCl), both drugs produced a marked reduction in PD, followed by acid back-diffusion and a small increase in GMBF, resulting in hemorrhagic lesions, and the effects again were more pronounced with alendronate. These irritative effects were dependent on the pH of drug solution and the action was more potent at pH 7 than pH 4. Conversely, the healing of acetic acid-induced gastric ulcers was significantly delayed by daily administration of these drugs, yet this effect was less pronounced in the case of risedronate. The healing impairing effect of these bisphosphonates was potentiated by coadministration of indomethacin. CONCLUSION: Both alendronate and risedronate have mucosal irritative and healing impairing effects in the stomach, yet the effect of risedronate was much less pronounced compared to alendronate. It is assumed that risedronate is safer than alendronate as the antiresorptive agent in patients with diseases related to bone remodeling.     

Gastric potential difference and pH in ulcer patients and normal volunteers during Stroop's colour word conflict test.

Whether mental stress is important in the pathogenesis of gastric mucosal disorders is not clearly established. This study investigated the relationship between sympathetic activation caused by the Stroop's colour word conflict test and gastric mucosal function, monitored by measuring the gastric mucosal electrical potential difference (PD). In 13 healthy volunteers and 12 duodenal ulcer patients gastric PD, pH, and heart rate were measured continuously during basal conditions, during mental stress evoked by the Stroop's colour word conflict test, and after return to basal conditions. The volunteers fell into two groups: In seven no sympathetic activation was elicited as no changes in heart rate were demonstrated. Gastric pH was unchanged, and PD increased slightly. Sympathetic activation was elicited in the other six with increased heart rate by 18 (6) beats per min. Potential difference declined significantly during sympathetic activation (delta PD = -5 (2)mV, p less than 0.05). Gastric pH increased. Eleven of 12 ulcer patients had sympathetic activation accompanied by a decline in PD, and an increased pH. Sympathetic activation in ulcer patients and volunteers impaired gastric mucosal function, as shown by a decline in gastric PD.     

Protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats

Objective:To observe the protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats.Methods:All rats were randomly divided into normal control group,cirrhosis and treatment group.Thioacetamide was used to establish rat model of cirrhotic portal hypertension.The necrotic tissue of gastric mucosa ulcer focus,degree of neutrophils infiltration at the ulcer margin,portal pressure,portal venous flow,abdominal aortic pressure,abdominal aortic blood flow at front end,gastric mucosal blood flow(GMBF),glycoprotein(GP)of gastric mucosa,basal acid secretion,H' back-diffusion,gastric mucosal damage index,NO,prostaglandin E_2(PGE_2) and tumor necrosis factor-α(TNF-α) were determined respectively,and the pathological changes of gastric mucosa were also observed by microscope.Results:Compared with cirrhosis group and the control group,the ulcer bottom necrotic material,gastric neutrophil infiltration and UI of the treatment group were all decreased significantly(P0.01),GMBF value,GP values,serum NO,PGE_2,TNF- a were all significantly increased.Conclusions:Omeprazole has an important protective effect on gastric mucosal and it can increase gastric mucosal blood flow and related to many factors.