Effect of dopamine on the healing of acetic acid-induced gastric ulcers in rats

Dopamine, as a neurotransmitter in the brain, is also present in the gastroduodenal mucosa and has been implicated in several functions in these tissues. Recent study showed that dopamine acts as a potent antitumor/angiogenic activity through suppression of growth factor expression. Since growth factors are known to play a crucial role in the mechanism of wound healing, it is possible that dopamine has a deleterious influence on the healing of gastric ulcers. In the present study, we examined the effect of dopamine on the healing of acetic acid-induced gastric ulcers in rats. Gastric ulcers were induced in male SD rats by serosal application of acetic acid for 60 sec. Dopamine was subcutaneously given twice daily for 7 days, starting 3 days after ulceration. In some case, the osmotic mini-pump filled with dopamine was implanted into the dorsal subcutaneous space in rats for 7 days. VEGF and Flk-1 mRNA expressions were determined by RT-PCR. Dopamine (3, 10 and 30 mg/kg) given subcutaneously for 7 days did not significantly affect the healing of gastric ulcers. The expression of VEGF and Flk-1 mRNA in the ulcerated mucosa was up-regulated after ulceration, and these expressions were not affected by dopamine. Likewise, dopamine (0.6 mg/kg/hr) infused continuously using the osmotic mini-pump also had no effect on the healing of these ulcers. These results suggest that dopamine, although reportedly shows a potent antitumor/angiogenic activity, does not cause any influence on the healing of the pre-existing gastric ulcers in rats. Received 3 August 2006; accepted 10 November 2006     

Effects of cimetidine on stress ulcer and gastric acid secretion in the rat

Cimetidine at 25, 50, and 100 mg/kg significantly inhibited gastric acid secretion in rats with chronic gastric cannulas. Rats receiving either 50 or 100 mg/kg of cimetidine secreted significantly less gastric acid 3 hr after injection. Cimetidine failed to reduce the number of size of gastric lesions in rats lesions in rats subjected to a supine restraint procedure.     

Influence of aging on gastric ulcer healing activities of cimetidine and omeprazole

In this study, we compared the effects of cimetidine and omeprazole on the healing of acetic acid-induced gastric ulcers in 8-, 48-, and 96-week-old rats. The repeated oral administration of cimetidine or omeprazole for 14 consecutive days markedly accelerated the ulcer healing in 8- and 48-week-old rats. However, both drugs were ineffective in 96-week-old rats. The basal gastric acid secretion of 8-, 48-, and 96-week-old rats decreased with aging. A single oral administration of cimetidine or omeprazole strongly decreased basal gastric acid secretion in the three different ages of rats. Cimetidine and omeprazole produced a potent and sustained serum gastrin-elevating action in 8- and 48-week-old rats. However, the gastrin-elevating actions of both drugs in 96-week-old rats were much weaker than in the 8- and 48-week-old rats. These results indicate that cimetidine and omeprazole have potent gastric ulcer healing actions in 8- and 48-week-old rats, as well as potent serum gastrin-elevating actions, but both drugs are ineffective in 96-week-old rats, which have lost their gastrin-elevating actions.     

The effects of metiamide on gastric secretion and stress ulceration in rats.

The effects of metiamide, a histamine H2 blocker, on gastric secretion and ulcer formation in stressed pylorus-occluded rats were investigated. Metiamide, like atropine, significantly reduced the volume of gastric secretion and total acid output in unrestrained pylorus-occluded rats. Both drugs produced greater decreases in the volumes of gastric secretion in stressed rats than in their corresponding unrestrained groups. Stress itself reduced both parameters. Metiamide, like atropine, significantly reduced the incidence of gastric stress ulcers. When given together these two drugs did not provide greater protection. The results obtained with metiamide indicate that histamine plays a role in basal gastric secretion and in the pathogenesis of stress ulcers. As no correlation between gastric acid secretion and ulcer formation was demonstrated in this study, it is suggested that H2 receptors may also be involved in gastric motility. However, the possibility that metiamide could exert its ulcer-protecting effects through other mechanisms cannot yet be excluded.     

胃、十二指肠溃疡合并大出血手术治疗体会

目的探讨胃、十二指肠溃疡合并大出血的治疗方法及疗效。方法回顾性分析本院近年来收治的胃、十二指肠溃疡合并大出血患者42例的临床资料,总结其治疗方法及疗效。结果 42例患者中41例治愈出院,治愈率为97.62%,住院时间12～33d,平均16.4d;死亡1例。发生并发症4例,占9.52%,其中切口感染2例,吻合口瘘2例。结论尽早手术是治疗胃、十二指肠溃疡合并大出血的首选方法,可有效止血,防止失血性休克的发生或进一步发展,提高患者的生存率。     

Antiulcerogenic activity of Scutia buxifolia on gastric ulcers induced by ethanol in rats

Gastric ulcers affect many people around the world and their development is a result of the imbalance between aggressive and protective factors in the gastric mucosa. Scutia buxifolia, commonly known as coronilha, has attracted the interest of the scientific community due to its pharmacological properties and its potential therapeutic applications. In this study, the preventive effects of the crude extract of Scutia buxifolia (ceSb) against gastric ulcer induced by 70% ethanol were evaluated in male Wistar rats. In addition, the composition of ceSb was clarified by high-performance liquid chromatography (HPLC). S. buxifolia extract (100, 200 and 400 mg/kg body weight) attenuated oxidative and histopathological features induced by ethanol. Moreover, all evaluated doses of ceSb caused significant (P<0.001 and P<0.0001) and dose-dependent increase in sulfhydryl groups (NPSH) levels, catalase (CAT) and superoxide dismutase (SOD) activities. Furthermore, the administration of ceSb reversed the increase in lipid peroxidation produced by ethanol. The protective effect of the extract could be attributed to antioxidant compounds present in the ceSb, such as flavonoids and phenolic acids, which were quantified by HPLC. Thus, an antioxidant effect of the extract leads to a protection on gastric tissue. These results indicate that S. buxifolia could have a beneficial role against ethanol toxicity by preventing oxidative stress and gastric tissue injury.KEY WORDS: Scutia buxifolia, Antioxidant, Gastric ulcer, HPLC     

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,     

Decreased acid secretion and gastric lesion production by morphine in rats

The effects of graded doses of morphine on gastric secretion were studied in conscious rats with pyloric occlusion. It was found that, at doses which significantly prolonged the reaction time in the tail-immersion test, morphine significantly decreased both the volume and total acid output of gastric secretion. It was also observed that morphine produced gastric mucosal lesions in a dose-dependent manner. Pretreatment with naloxone 4 mg/kg significantly alleviated the gastric effects of morphine 32 mg/kg. It is suggested that the depressant effects of morphine on gastric secretion and the ulcerogenicity of the narcotic result from its stimulant activity on opiate receptors.     

The role of zinc ion in the development of gastric ulcers in rats

The properties of the gastric mucosal barrier and acid output were investigated in zinc deficient rats. A decline in total acid output, a significant diminution in hydrogen and sodium ion fluxes and an increase in gastric lesions suggest a marked breakdown of the gastric mucosal barrier in zinc deficient rats.     

Effects of alkyl analogs of histamine and metiamide on gastric acid secretion.

Histamine and metiamide analogs with alkyl, methyl, ethyl or isopropyl groups on the imidazole ring in position 5, not previously tested on an in vivo preparation, were studied for their effects on gastric acid secretion in cats with gastric fistulas. Our findings confirmed that the methyl group appears to be optimal for an effect on gastric acid secretion as regards both agonism and antagonism. Ethyl substitution apparently did not change the pharmacological activity of histamine but modified the inhibitory effect of metiamide from competitive to non-competitive kinetics. Isopropyl analogs were inactive on gastric secretion under our experimental conditions.     

Autonomic drug effects and gastric secretion in a new experimental model of stress ulcers in rats

A psychological procedure which does not involve the application of physical stimulation was used to produce gastric ulcers experimentally. Ulceration was induced in rats by exposing the animals to the aggressive attacks of rats treated with 6-hydroxy-dopamine (6-OHDA). Gastric secretion and the effects of autonomic drugs on ulcer formation were investigated. Atropine methylbromide did not significantly inhibit the occurrence of erosions. Phentolamine or hexamethonium bromide significantly inhibited the production of erosions, and combined administration of an anticholinergic agents and alpha-blocking agent led to a complete inhibition, with no notable behavioral change. In case of pylorus ligation, gastric secretion during exposure to attack of 6-OHDA-treated rats was significantly less than that in the controls. We suggest that the sympathetic nervous system plays an important role in the production of gastric erosions, as induced by the methods reported in this study.     

Effect of intravenous atropine and methylatropine on heart rate and secretion of saliva in man

Summary Intravenous atropine sulphate (0.25, 0.40, 0.75 and 1.50 mg), atropine methylnitrate (0.08, 0.13 and 0.25 mg) and saline were given to 72 healthy medical students. The effects on heart rate and rhythm, systolic and diastolic blood pressure and salivary secretion were studied. Salivation was inhibited by all the doses of the two drugs. There was a clear dose-response relationship and methylatropine was about 3 times as potent as atropine. Heart rate was accelerated by 0.75 and 1.50 mg atropine, and 0.25 mg methylatropine, whereas 0.25 mg atropine and 0.08 and 0.13 mg methylatropine induced bradycardia, which was considered to be due to a peripheral action. It is suggested that the drugs act as partial agonists at muscarinic receptors. No clear effect on blood pressure was seen, except for the highest dose of atropine, after which the diastolic pressure was increased. 20 out of 59 subjects who received anticholinergics developed supra-ventricular arrhythmias; with both drugs periods of nodal rhythm were most common. They appeared shortly after the injection and usually lasted for a few minutes.     

慢性胃、十二指肠溃疡患者的心理护理及体会

目的 总结对慢性胃、十二指肠溃疡患者的心理护理体会,以供参考.方法 以我院收治的慢性胃、十二指肠溃疡患者157例为研究对象,随机分组.对照组给予常规护理干预,观察组在此基础上加强心理护理,观察护理干预前后患者情绪变化,并比较护患满意率的差异.结果 护理干预后两组患者SAS评分、SDS评分均较干预前下降;与对照组相比较,观察组干预后SAS评分、SDS评分较低,差异有统计学意义（P＜0.05）.对照组护患满意率为92.31％,观察组护患满意率为100.00％,与对照组相比较,观察组护患满意度较高,差异有统计学意义（P＜0.05）.结论 重视对慢性胃、十二指肠溃疡患者进行心理护理,有助于改善患者情绪状态,促进疾病康复,并可增进护患关系,具有积极的临床意义.     

Effects of ethanol on the secretion and mucosal blood flow of a denervated gastric pouch in the dog.

Mucosal secretion and blood flow of a Heidenhain pouch were measured in dogs after orally administered ethanol at doses from 0.25 to 2 g/kg of body weight. Under these conditions, the volume, free and total acidity of the gastric juice as well as mucosal blood flow increased linearly with the dose up to 1 g/kg. In all cases volume secreted and acidity chanm the other parameters and could not be correlated with blood flow. The influence of gastrin and the modification of membrane permeability are discussed with regard to these data.     

Cholinergic control of gastric acid secretion

Summary In the perfused stomach preparation of the anaesthetized rat the cholinergic agonists acetylcholine (ACh) and bethanechol stimulated gastric acid secretion. Both agonists produced similar maximal acid output (70 mol/15 min) when infused intravenously. However, bethanechol was more potent, eliciting half maximal stimulation at 1.98 mol/kg/h. Secretory responses to either agonist were antagonized in a dose related fashion by blockade of muscarinic receptors with atropine. In contrast, inhibition of nicotinic receptors with hexamethonium produced a striking potentiation of ACh stimulated secretion whilst the bethanechol elicited secretion remained unaffected. In the presence of full nicotinic receptor blockade the ACh response curve was shifted to the left sixfold, half maximal stimulation being produced at 1.79 mol/kg/h. Cimetidine partially inhibited the secretory responses elicited by either ACh or bethanechol while blockade of adrenoceptors ( and ) did not affect acid output induced by cholinergic agonists. Secretion elicited by ACh is interpreted as being the composite effect of prosecretory action and an inhibitory mechanism due to the activation of nicotinic receptors. Hexamethonium, through nicotinic receptor blockade, inhibits the restricting mechanism and thus reveals the full stimulatory action of ACh.     

胃灵冲剂对大鼠乙酸胃溃疡愈合质量的影响

目的 研究胃灵冲剂对大鼠胃溃疡愈合质量的影响.方法 用冰醋酸制备大鼠慢性胃溃疡模型,随机分为5组,分别灌胃胃灵冲剂(2.4、4.8、9.6g·kg-1)、雷尼替丁、生理盐水.用阿利斯蓝染液对胃壁结合粘液进行测定;注墨汁法测量溃疡体积.结果 胃灵冲剂各剂量组的胃壁结合粘液量高于生理盐水组;胃灵冲剂(4.8、9.6g·kg-1)组的溃疡面积明显小于生理盐水对照组.结论 胃灵冲剂能促进冰醋酸胃溃疡愈合.     

The influence of cimetidine,a histamine H2-receptor antagonist,on the gastric effects of reserpine in rats

The effects of the graded doses of cimetidine on both resting and reserpine-evoked gastric acid secretion were examined in relation to their influence on reserpine-induced ulceration, mast cell degranulation and mucosal microcirculatory changes in rat stomachs. Cimetidine 10 mg/kg or above reduced resting or reserpine-provoked gastric acid secretion as well as rumenal and glandular ulceration. However, non-acid-inhibiting doses, 5 mg/kg or below, continued to prevent glandular ulceration. Reserpine-evoked gastric glandular mucosal mast cell degranulation was unaffected by both acid-inhibiting and non-acid-inhibiting doses of cimetidine which dose-dependently blocked the superficial glandular mucosal microcirculatory volume changes. These results suggest that cimetidine prevents reserpine-induced glandular ulceration largely by blocking the ulcerogenic effect of histamine H₂-receptor-mediated mucosal microcirculatory congestion, in contrast to antagonising rumenal lesions through acid inhibition; they also support the idea that reserpine may release histamine mainly from the glandular mucosal mast cells. The possibility of another antiulcer mechanism, due to cytoprotection, is discussed.     

Effect of metiamide, a histamine H2 - receptor antagonist, on the development of gastric stress ulcers and acid secretion.

In normal and stressed rats with chronic gastric fistula small doses of metiamide (0.001-0.01 muM/kg) increased and doses of over 20 muM/kg decreased gastric acid secretion. In both these dose ranges of dosage metiamide suppressed the development of stress ulcers, most markedly in doses of 0.005 and 100 muM/kg. Intermediate doses had no such action. Only the anti-ulcer action of large doses of metiamide ran parallel to a reduction in acid secretion. Small doses of metiamide increased gastric secretion, but like larger doses, had a weak adrenergic action.