沙棘油乳抗大鼠慢性萎缩性胃炎和胃溃疡作用研究

目的 :研究沙棘油乳抗大鼠慢性萎缩性胃炎和胃溃疡作用。方法 :采用动物的萎缩性胃炎、胃溃疡模型 ,评价沙棘油乳的抗萎缩性胃炎、胃溃疡作用。结果 :沙棘油乳能明显防止脱氧胆酸钠和应激所致慢性萎缩性胃炎、胃溃疡 ;对大鼠幽门结扎引起的急性胃溃疡指数有显著降低作用 ;对小鼠消炎痛 -乙醇性溃疡有显著对抗作用。结论 :沙棘油乳具有制酸、保护胃粘膜的作用     

蒲葛舒胃灵对实验性胃溃疡作用的研究

目的研究蒲葛舒胃灵抗实验性胃溃疡的作用。方法采用应激性胃溃疡模型、吲哚美辛致大鼠急性胃黏膜损伤模型、大鼠幽门结扎胃溃疡等模型观察蒲葛舒胃灵抗胃溃疡作用、对醋酸所致小鼠扭体反应的影响和体外抗幽门螺杆菌的作用。结果蒲葛舒胃灵能减少大鼠实验性胃溃疡面积,抑制醋酸所致小鼠扭体反应次数,对幽门螺杆菌具有明显抑制作用。结论蒲葛舒胃灵有显著的抗胃溃疡作用,实验结果与该药用于治疗胃溃疡的功效吻合。     

血清抗幽门螺杆菌热休克蛋白60抗体与消化性溃疡的关系

目的：探讨幽门螺杆菌(Hp)感染患者血清抗幽门螺杆菌热休克蛋白60(Hsp 60)抗体与消化性溃疡的关系。方法：检测胃溃疡、十二指肠球部溃疡、慢性浅表性胃炎患者Hp感染及血清抗幽门螺杆菌Hsp60抗体表达情况。结果：(1)血清抗幽门螺杆菌Hsp60抗体阳性表达仅见于Hp阳性患者。Hp阳性胃溃疡、十二指肠球部溃疡患者血清抗幽门螺杆菌Hsp抗体阳性率明显高于慢性浅表性胃炎患者(均P＜0．05)。(2)26例血清抗幽门螺杆菌Hsp抗体阳性的消化性溃疡患者在Hp根除及洛赛克疗程结束后4周，其中7例抗体转为阴性。结论：血清抗幽门螺杆菌Hsp60抗体可能与Hp感染所致消化性溃疡的发生有关；血清抗幽门螺杆菌Hsp60抗体不能作为近期判断Hp根除与否的标准。     

欧达胃克抗溃疡作用的实验研究

以欧达胃克162mg/kg或法莫替丁3.6mg/kg经大鼠灌胃对抗胃溃疡(由吲哚美辛诱导的)和应激性溃疡模型均有明显的保护作用。二药对两种溃疡的抑制率分别为69.5％对71.5％和77.7％对42.7％。又以同样方式对抗乙酸诱导的胃溃疡,其抑制率分别为82.6％和59.6％,实验药的保护作用明显优于对照药。体外试验证明,实验药对幽门螺杆菌(Hp)的抑制作用优于对照药丽珠得乐。欧达胃克抑制慢性溃疡的作用可能与促进上皮细胞和肉芽组织生长及抑制Hp有关。     

参香养胃胶囊的抗溃疡药效学研究

目的:研究参香养胃胶囊抗SD大鼠胃溃疡及抗胃黏膜损伤的作用。方法:采用水浸应激法、幽门结扎法、利血平法、醋酸等方法致大鼠胃溃疡,盐酸-乙醇、吲哚美辛致大鼠急性胃黏膜损伤,进行抗胃溃疡和胃黏膜保护实验。结果:参香养胃胶囊能明显抑制水浸应激、幽门结扎、利血平以及醋酸致大鼠胃溃疡;并对盐酸-乙醇、消炎痛所致大鼠急性胃黏膜损伤有明显的抑制作用;结论:参香养胃胶囊具有抗溃疡的作用。     

复方尿囊素片治疗胃溃疡疗效及机制研究

胃溃疡是一种慢性复发性病变,严重危害身体健康,其病因复杂。现代医学认为,胃酸过高,黏膜保护作用减弱和幽门螺杆菌(Hp)感染等是产生胃溃疡的主要原因。因此在抑酸及根除Hp治疗胃溃疡的同时,应给予增强黏膜屏     

安胃微丸抗胃溃疡作用

目的考察安胃微丸对慢性胃溃疡的治疗作用及对急性胃溃疡的保护作用。方法采用大鼠醋酸烧灼法、幽门结扎法和小鼠水应激法及消炎痛法 4种胃溃疡动物模型。结果安胃微丸对醋酸侵袭胃壁所致慢性胃溃疡有明显的治疗作用 ,对大鼠幽门结扎有一定保护作用 ,并能明显抑制胃酸及胃蛋白酶活性 ,对消炎痛引起的小鼠药物性胃溃疡有显著的抑制作用 ,并能抑制水浸应激性胃溃疡。并显示其有一定的镇痛作用。结论安胃微丸有很好的抗胃溃疡作用。     

奥美拉唑抗实验性胃溃疡的作用

观察了国产奥美拉唑抗实验性胃溃疡的作用。奥美拉唑能明显抑制阿斯匹林所致小鼠胃溃疡、小鼠应激性胃溃疡和组胺所致豚鼠胃溃疡，其抗溃疡作用强于同剂量的盐酸雷尼替丁。     

左旋泮托拉唑镁对动物实验性胃溃疡的影响

目的研究左旋泮托拉唑镁 ((- ) PAN·Mg)对动物实验性胃溃疡的影响。方法应用小鼠束水应激型胃溃疡模型、小鼠阿斯匹林型胃溃疡模型、大鼠醋酸烧灼型胃溃疡模型、大鼠幽门结扎型胃溃疡模型 ,急性胃瘘大鼠模型 ,观察口服 (- ) PAN·Mg对胃溃疡的抑制作用及对胃酸分泌的影响 ,并与右旋、消旋体进行了比较。结果 (- ) PAN·Mg对动物实验型胃溃疡具有明显的保护作用 ,能显著抑制溃疡的发生 ,抑制胃酸分泌 ,对胃溃疡的抑制效果优于 (+) PAN·Mg和 (± ) PAN·Mg。 结论 (- ) PAN·Mg的抗动物实验性胃溃疡作用和抑酸作用强于右旋 ((+) PAN·Mg)与消旋泮托拉唑镁 ((± ) PAN·Mg) ,具有良好的新药开发前景     

醋氨己酸锌抗实验性胃溃疡作用

对醋氨己酸锌的抗实验性动物胃溃疡作用进行了研究，结果表明，醋氨己酸锌显著的抑制小鼠水浸应激性胃溃疡形成，对无水乙醇所致的大鼠胃粘膜损伤具有明显的保护作用，且显著减轻幽门结扎大鼠胃粘膜的损伤，同时，对大鼠幽门结扎大后６ｈ的胃液进行分析，３００ｍｇ／ｋｇ醋氨己酸锌增加胃液分泌量，降低游离酸和总酸量，醋氨己酸锌并具有抑制胃蛋白酶活性的作用。     

Effect of metiamide, a histamine H2-receptor antagonist on reserpine-induced gastric ulcers and acid secretion

The effect of metiamide on reserpine-induced gastric ulcers and on gastric secretion during 6 h after ip administration was investigated in conscious intact rats and in rats with chronic gastric fistula. Reserpine, 3 mg/kg ip increased substantially the concentration of gastric acid in the first 4 h. Metiamide given every 3 h in a low dose (0.01 mumol/kg) intensified reserpine-induced gastric ulcers and also significantly increased the reserpine-induced acid concentration and output. In larger doses, (50-100 mumol/kg) metiamide considerably diminished gastric ulcer development and decreased gastric acid concentration. Given every 2 h metiamide in doses of 50-100 mumol/kg almost completely abolished gastric ulcer formation and markedly reduced the secretion of gastric acid in reserpinized rats. Anti-ulcer effect of metiamide was stronger than its antisecretory action, suggesting also the antiulcer action of metiamide other than inhibition of acid secretion. The results suggest that in conscious rats histamine H2-receptors are involved in reserpine-induced gastric ulcer development and gastric acid secretion. The antiulcer effect of metiamide may in part depend on its antisecretory action.     

Healing-promoting action of rhinax with dual action on chronic gastric and duodenal ulcers induced by acetic acid in rats

Healing promoting actions of Rhinax, a multiconstituent herbal preparation, was investigated in chronic gastric and duodenal ulcer models induced by acetic acid in rats and the effects were compared with those of famotidine by gross of histological evaluation. Rhinax markedly promoted the well balanced healing of gastric ulcer at oral does of 25-100 mg/kg x 2 /day, as evidenced by the reduction of ulcer, regeneration of mucosa and proliferation of connecitve tissue. Rhinax caused an increase in gastric mucosa secretion in all the regenerated mucosa around the gastric ulcers. Famotidine failed to promote the healing of gastric ulcers at 100 mg/kg x 2/ day p.o. Rhinax also significantly accelerated the healing of acetic acid -induced duodenal ulcers as well famotidine. These results indicate that Rhinax is characterised by a potent promoting action on the healing of chronic ulcers, suggesting that the increase in gastric mucus secretion might be associated with the antiulcer action of Rhinax in rats.     

Antiulcer activity of levcromakalim and nicorandil in albino rats: a comparative study

The objective of the present study was to investigate and compare the antiulcer effect of potassium channel openers, nicorandil and levcromakalim in the models of ulcer induced by pylorus ligation, aspirin and water immersion plus restraint stress in albino rats. Levcromakalim (250 microg/kg) and nicorandil (10 mg/kg) were administered intraduodenally immediately after pylorus ligation. Ulcer index was determined and gastric juice was subjected to analysis of total acid output (TAO) and pH. In aspirin-induced gastric ulcer model, the drugs were administered orally 30 min prior to noxious challenge, and in water immersion restraint stress model, the drugs were administered orally and ulcer index was determined. A significant reduction in ulcer index was observed after treatment with both potassium channel openers in all the gastric ulcer models. In pylorus-ligated rats, a significant decrease in TAO was noted. The conclusion is that potassium channel openers possess antiulcer activity. Antiulcer activity of levcromakalim is better than nicorandil but comparable to that of cimetidine. The antiulcer action of potassium channel openers is mediated partially by a decrease in gastric acid secretion, increase in gastric mucosal resistance and improvement in gastric mucosal blood flow.     

脑室注射催产素对大鼠胃和十二指肠溃疡的作用

INTRODUCTION Central neurons that synthesize oxytocin are locatedin the supraoptic(SON) and paraventricular nuclei(PVN) of the hypothalamus. Magnocellular neurons inboth nuclei project to the posterior pituitary gland,     

大蒜素抗溃疡及通便作用研究

目的研究大蒜素抗溃疡作用和对排便作用的影响。方法采用乙醇/盐酸大鼠胃溃疡模型、幽门结扎型溃疡模型、消炎痛致溃疡模型及乙酸致胃溃疡等模型,观察动物溃疡指数;采用燥结失水便秘模型,观察动物排便时间及排便点数;采用正常小鼠碳末推进实验,观察小鼠小肠运动功能。结果大蒜素能减少乙醇/盐酸大鼠胃溃疡模型、幽门结扎型溃疡模型、消炎痛致溃疡模型及乙酸致胃溃疡等模型的溃疡指数(P<0.05或P<0.01);能使模拟燥结的失水便秘模型小鼠的排便时间缩短,排便点数增加(P<0.05或P<0.01);能增加正常小鼠小肠碳末推进的百分率(P<0.05或P<0.01)。结论大蒜素具有抗溃疡及促进排便作用。     

Luminal acid in stress ulceration and the antiulcer action of verapamil in rat stomachs

The role of luminal acid and the influence of the antisecretory action of verapamil in stress ulcer prevention in rat stomachs have been studied. Intraperitoneally injected verapamil, 4 mg kg-1, inhibited gastric acid secretion and ulcer formation, however, a 2 mg kg-1 dose, which did not significantly influence acid output, also had an antiulcer effect. Intraperitoneal injection of bethanechol, 1.2 or 3.6 mg kg-1, increased gastric acid output, but did not influence stress-induced ulcer formation. Oral administration of HCl, 25 or 50 mu equiv, aggravated stress ulceration in a dose-dependent manner; this lesion-worsening effect was prevented by pretreatment with verapamil or bethanechol. The gastric luminal acid content in 2 h pylorus-ligated rats was similar in the groups given either bethanechol or HCl. These findings indicate that the antisecretory action of verapamil may not account for its antiulcer effect. It is suggested that endogenous and exogenous luminal acid may have different influences on stress ulcer formation.     

锁阳多糖对实验性急性胃溃疡大鼠模型的影响

目的研究锁阳多糖对急性胃溃疡大鼠模型的影响。方法采用水浸束缚应激、幽门结扎致胃溃疡两种模型,观察锁阳多糖对大鼠急性胃溃疡的预防作用。结果与模型组比较,锁阳多糖高、中剂量组能抑制水浸应激性大鼠胃溃疡的形成,溃疡抑制率分别为37.7%、26.2%(P<0.01);同时锁阳多糖高、中、低剂量组能降低幽门结扎型大鼠胃溃疡指数,溃疡抑制率分别为42.0%、23.3%、16.3%(P<0.05,P<0.01)。结论锁阳多糖具有抗急性胃溃疡作用,其机制与改善胃黏膜的微循环,增强胃黏膜防御能力有关。     

Effects of FRG-8701 on gastric acid secretion, gastric mucosal lesions by necrotizing agents and experimental gastric or duodenal ulcer in rats

Effects of FRG-8701, a new histamine H2-receptor antagonist, on gastric acid secretion, necrotizing agents-induced gastric lesions and acute gastric or duodenal ulcer in rats were studied. In lumen-perfused rats, intravenous injection of FRG-8701 reduced gastric acid secretion, and its antisecretory effect was almost equipotent to that of famotidine but the duration of action was substantially longer. In pylorus-ligated rats, the antisecretory effect of intraduodenal FRG-8701 administration was about 7 times more potent than that of cimetidine. FRG-8701 effectively inhibited macroscopic gastric hemorrhagic lesions induced by various kinds of necrotizing agents. Intraperitoneal injection was effective in preventing the lesions as well as oral treatment. The oral ED50 values for these lesions ranged from 1.1 to 9.4 mg/kg. On the other hand, famotidine failed to reduce these lesions, and the cytoprotective effect of cimetidine was observed only in high doses compared with the doses for antisecretory activity. In addition, the cytoprotective effect of FRG-8701 was not affected by the treatment of indomethacin or N-ethylmaleimide. FRG-8701 showed antiulcer activity against stress and indomethacin gastric ulcer and mepirizole duodenal ulcer. Its antiulcer effect was 5-15 times more potent than that of cimetidine. These results indicate that FRG-8701 is a new antiulcer drug that exerts a potent cytoprotective effect in addition to its gastric antisecretory activity.