[Argentinean registry on the management of Helicobacter pylori infection: effectiveness and safety of first line treatment].

Introduction: The optimal management of Helicobacter pylori (H pylori) infection remains unclear. Updated information concerning local data is needed to design the best strategy to treat H. pylori infection to reach high eradication rates.

[Metaplasic Paneth cells in ulcerative colitis].

Background: Paneth cells are normally present in small intestine, but its appearance in other areas of the gastrointestinal tract is related to chronic inflammatory processes.

Material And Methods: In our study we retrospectively examined 29 patients with diagnosis of ulcerative colitis, from the files of Instituto de Histopatología de Rosario, and from the casuistry of two authors (O.B.

In vivo selectivity of nonsteroidal antiinflammatory drugs and gastrointestinal ulcers in rats.

The aim of the present work was to study in vivo COX-2-COX-1 selectivity of 16 nonsteroidal anti-inflammatory drugs (NSAIDs) in equipotent ulcerogenic doses in two in vivo experimental models. Indomethacin, ibuprofen, nimesulide, aceclofenac, aspirin, sodium diclofenac, meloxicam, naproxene, paracetamol, piroxicam, tenoxicam, nabumetone, ketoprofen, mefenamic acid, etodolac, and ketorolac were administered to female Wistar rats (N = 10 each group). In experiment I, solid food plus subcutaneous NSAIDs were given.

[Autonomic nervous system and gastric stress in rats].

The role of the autonomic nervous system on gastric stress was studied in different groups of Wistar rats (n = 10). The experimental stress model consisted of immobilization and immersion in 15 degrees C water during 6 hours. The percentage of the gastric mucosa macroscopic lesional area was tabulated, and at the same time cortisol, melatonin, noradrenaline, adrenaline, dopamine and serotonin blood levels were measured.

[In vivo selectivity of nonsteroidal anti-inflammatory drugs on COX-1-COX-2 and gastrointestinal ulcers, in rats].

Unlabelled: This work was aimed to study COX-1 and COX-2 selectivity in 16 non-steroidal anti-inflammatory drugs (NSAIDs), at ulcerogenic doses in 2 experimental models: 1) provided subcutaneously (sc), after solid food(SF), (antrum ulcers and intestinal erosions); and 2) orally (O) (fundic and intestinal erosions).

Methods: 17 groups of female Wistar rats (n = 7 each group), weighing 200 g, 36 h fasting with water ad libitum, were submitted to the following experiments: 1. SF (Cargill chow) during 1 h, and then sc: 1.

[Role of inducible nitric oxide synthase in acute gastric mucosal damage in stress, in rats].

In groups of female Wistar rats, someted to stress by immobilization and immersion in 18 degrees C water during 6 hrs, the role of nitric oxide (NO) in its pathophysiologic was studied. Agonist and antagonist of the isoforms Constitutive NO Synthase (cNOS) and of the inducible NO Synthase (iNOS) were used. Was found that the overdose of L-arginine aggravated of stress acute gastric lesions.

[Evaluation of treatment for the prevention of acute gastric lesions in stress, in rats].

Objective: To verify wether a cytoprotective or a antisecretant drug is effective on stress acute gastric.

Method: Female Wistar rats (n=7), 200 g, 24 h fasted, water ad lib. were used.

Sucralphate in the prevention of acute gastric lesions induced by ischemia-reperfusion.

The role of sucralphate in prevention of acute gastric injuries and its comparison with free radical blockers such as allopurinol, soybean trypsin inhibitor and superoxidase dismutase in the ischemia-reperfusion model by total occlusion of the coeliac artery in Wistar rats, was studied. The gross gastric mucosal necrotic area was 80%. In contrast with the antioxidant drugs the necrotic area attained was between 7 to 15%, while with sucralphate, an antioxidant-cytoprotective drug that enhances the gastric defensive barrier, the prevention of the secondary aggression induced by free radicals was more important.

[Role of ACE in the gastric cytoprotection. Dopaminergic and peripheral alpha 2 adrenergic mechanisms].

In Wistar rats, four experiments were carried out, studying specific inhibitors for ACE (angiotensin-converting enzyme), such as captopril, enalapril, lisinopril, ramipril and cilazapril, in presence of 20% and 95% ethanol induced gastric lesions. The effect of lisinopril and angiotensin I on the same injury was also studied. Subsequently, drugs with known role in gastric mucosa cytoprotection, such as enprostil, paracetamol, ketotiphen, levamisole, diazepam, bromocriptine, dopamine and clonidine, before and after absolute ethanol gastric injury were also studied.

Sucralfate in the prevention of acute gastric lesions induced by ischemia-reperfusion.

The role of Sucralfate in prevention of acute gastric injuries and its comparison with free radicals blockers as Allopurinol, Soybean Trypsin Inhibitor and Superoxide Dismutase was studied in the ischemia-reperfusion model by total occlusion of the celiac axis in Wistar rats. In control rats, the gross gastric mucosal necrotic area was of 80%; in contrast, the antioxidant drugs resulted in a necrotic area of 7%-15% and Sucralfate resulted in a necrotic area of only a 4%. It was concluded that Sucralfate, as antioxidant-cytoprotective drug, by enhancing the gastric defensive barrier was more important than the secondary aggression induced by free radicals.

Evidence of anti-oxidant role of sucralfate in gastric mucosal protection.

Six percent hydrogen peroxide (H2O2) was used as a generator of the *OH free radical, and as an aggressor of gastric mucosa, in 100 Wistar rats. The mucosal cytoprotector effect of sucralfate, misoprostol, enprostil, cimetidine, ranitidine, famotidine and 10% aluminum sulphate yielded almost complete macroscopic and histological protection to the gastric mucosa. Misoprostol or enprostil gave partial protection whereas the H2 blockers aggravated the gastric necrotic lesions produced by the H2O2.

[Role of protons and bicarbonate in adaptative gastric cytoprotection].

The unknown mechanism of adaptative gastric cytoprotection (AGC) induced by 20% ethanol and subsequent injury with 70% ethanol was studied in wistar rats. Pretreatment with indomethacin or HgII2 did not prevent the AGC, there suggesting that neither endogenous PGS nor gastric mucus take part in its mechanism. On the other hand, ranitidine pretreatment blocked and even aggravated the damage induced by ethanol-ethanol.

[Pathogenic aspects of duodenal ulcers by cysteamine. Role of the Brunner glands].

In Wistar rats, the acid factor, the peripheral dopaminergic mechanism and the role of Brunner gland (BG), in the prevention of the Cysteamine duodenal ulcer (CDU) were studied. It was found that Bromocriptine; a peripheral dopaminergic neuronal receptor agonist (DA2), produced prevention of the CDU and blocked of PAS depletion of the BG; in contrast, SCH23390, a peripheral dopaminergic vascular receptor antagonist (DA1), and SAMe, a peripheral and central antidopaminergic; induced aggravation of CDU and total depletion of the BG. In conclusion, the HCl factor, a peripheral dopaminergic mechanism and impaired Brunners gland secretion of PAS mucus, in the pathogenesis of the CDU was postulated.

Gastric cytoprotection induced by prostaglandin-dopaminergic mechanism.

The cytoprotective effects on the gastric mucosa of the Bromocriptine, a peripheral dopaminergic receptor agonist compared with Misoprostol against ethanol-induced injury were studied. Pretreatment with SCH 23390 (a DA1 receptor antagonist) and Domperidone (a DA2 receptor antagonist), showed that Misoprostol was peripheral dopaminergic receptor dependent in the gastric cytoprotective mechanism, and that Bromocriptine was a selective peripheral DA2 receptor agonist in the gastric cytoprotection mechanism; as well as, indomethacin pretreatment, showed that peripheral DA2 receptors were endogenous prostaglandin dependent. In conclusion, a prostaglandin-dopaminergic mechanism was postulated in gastric cytoprotection.