Unlabelled: The immunomodulator effect of Bioflora probiotic on T (CD4+) and B (CD20) lymphocytes in gastrointestinal mucosa and intestinal bacterial translocation was studied using Wistar rats (n = 10 per group). Two experiments were used: (I) stress with immobilization and water immersion at 22 degrees C for 7 h plus the application of indomethacin (Indo) 10 mg/kg SC every 24 h for 3 days (comparator group), and (II) stress experiment I with the addition of 1 mL of Bioflora applied through a orogastric tube every 12 h for 3 days. At the 4th day, in asepsis, a dissection laparotomy of liver, spleen, mesenteric lymphatic nodes, and cecum was performed for microbiological culture, and stomach, ileum, and colon were also dissected for immunohistochemical and quantification of CD4+ and CD20.
View Article and Find Full Text PDFThe anti-inflammatory effect of Bioflora probiotic administered orally or subcutaneously with viable or nonviable bacteria was analyzed in two experimental models of randomly selected female Wistar rats. The use of indomethacin at a dose of 50 mg/kg was associated with gastric necrotic lesions and multiple erosions of the small intestine, with marked mucosal neutrophil infiltrate measured by myeloperoxidase (MPO). Probiotics prevented both gastrointestinal lesions and neutrophil infiltrate (p < 0.
View Article and Find Full Text PDFActa Gastroenterol Latinoam
June 2006
Background: The antiinflammatory and gastric cytoprotector effect of angiotensin II AT1 receptor antagonist, such as candesartan, losartan and valsartan was studied.
Material And Methods: Wistar rats were ramdomly assigned to receive: (1) 96 degrees ethanol; (2) oral indometacin, (3) solid food (pellets) during two hours and subcutaneous indometacin (production of ulcers in the gastric antrum), (4) Carrageen footpad edema.
Results: The three ATI receptor angiotensin antagonists yielded gastric cytoprotection against 96 degrees ethanol, almost total gastrointestinal protection against oral indometacin, prevented gastric ulcers formation in the antrum induced by subcutaneous indometacin, remarkable antiinflammatory response against neutrophil infiltration on the gastrointestinal mucosa, and anti-inflammatory effect in carrageen footpad edema.
Acta Gastroenterol Latinoam
May 2004
In randomized groups of Wistar rats, the effect inhibitor of selective NASAID over the COX-1, COX-2 and COX-3 the synchronizes inhibition of COX-1 and COX-2, COX-1 and COX-3, COX-2 and COX-3, and COX-1, COX-2 and COX-3 were studied. The conclusions were that the selective inhibition of COX-1, COX-2 and COX-3 no given gastrointestinal damage; the synchronizes inhibition of COX-1 and COX-2 given preferential gastric damage; in contrast the inhibition of COX-2 and COX-3 given massive necrosis preferential in small intestine.
View Article and Find Full Text PDFActa Gastroenterol Latinoam
May 2002
Dexketoprofene (De) NSAID was studied as a selective COX-1 inhibitor in comparison with Ketorolac (Ke), a mainly COX-1 inhibitor. De and Ke were administered to different groups of animals in a dose-dependent manner, i.e.
View Article and Find Full Text PDFFive experimental models were developed in different groups of Wistar rats (N = 15) to study selective COX-2-inhibitor NSAIDs such as celecoxib and rofecoxib, as follows: (1) dose-dependent oral Celecoxib and Rofecoxib for 5 days, and 24 hr after oral indomethacin; (2) Same as 1 but subcutaneously; (3) gastric ulcer induced by glacial acetic acid; (4) duodenal ulcer induced by cysteamine; and (5) stress by immobilization and immersion in water at 15 degrees C for 6 hr. Celecoxib and Rofecoxib, either orally or subcutaneously, did not produce necrotic lesions in healthy gastrointestinal mucosa (0%), showing normal histology. In contrast, previously indomethacin-induced lesions were aggravated (90%, P < 0.
View Article and Find Full Text PDFIn 5 random groups of Wistar rats (n = 15 for each group), ulcerogenic doses of NSAIDs COX-1-COX-2 inhibitors such as indomethacin were compared with Celecoxib (COX-2 inhibitor); the production of antrum gastric ulcers and bowel and colon necrotic areas was studied. Celecoxib was given each 12 hs orally and subcutaneously during 5 days and gastrointestinal lesions were not found; in contrast, Celecoxib given after indomethacin aggravated antrum gastric ulcers (p < 0.001); intestinal massive necrosis and death were observed in all the rats.
View Article and Find Full Text PDFThe 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.
View Article and Find Full Text PDFActa Gastroenterol Latinoam
July 2000
Unlabelled: Five experimental models were carried out in different groups of Wistar rats (n = 15) in order to study selective (cyclo-oxygenase) COX-2 non-steroid antiinflammatory inhibitors, such as celecoxib and rofecoxib, as follows: 1) Dose-dependent oral celecoxib and rofecoxib for 5 days, and 24 hours after oral indomethacin. 2) Same as 1, but subcutaneously. 3) Gastric ulcer induced by means of glacial acetic acid.
View Article and Find Full Text PDFActa Gastroenterol Latinoam
October 1998
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.
Acta Gastroenterol Latinoam
March 1998
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.
View Article and Find Full Text PDFActa Gastroenterol Latinoam
May 1996
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.
The effect of Molsidomine as a gastric mucosa protector against absolute ethanol was studied in Wistar rats. It was found that Molsidomine provided an important gastric cytoprotection and it behaved in a similar way as the nitric oxide (NO), the latter verified by specific NO antagonist, namely the NG-monomethyl-L arginine. It was also demonstrated that the cytoprotector mechanism of Molsidomine, as well as of other nitroderivates was sulfhydryl and HEM dependent regarding the guanylate-cyclase enzyme.
View Article and Find Full Text PDFItal J Gastroenterol
September 1992
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.
View Article and Find Full Text PDFActa Gastroenterol Latinoam
May 1993
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.
View Article and Find Full Text PDFActa Gastroenterol Latinoam
August 1992
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.
View Article and Find Full Text PDFItal J Gastroenterol
February 1990
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.
View Article and Find Full Text PDFActa Gastroenterol Latinoam
February 1991
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.
View Article and Find Full Text PDFRev Esp Enferm Apar Dig
March 1988
Acta Gastroenterol Latinoam
January 1990
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.
View Article and Find Full Text PDFActa Gastroenterol Latinoam
February 1989
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.
View Article and Find Full Text PDFIn groups of white Wistar rats, the cytoprotective effect induced by TDB on the gastric mucosa against the ethanol injury, was studied; where macroscopic protection and histologic cytoprotection in gastric corpus was found, and no in antrum mucosa. The cytoprotective mechanism give by TDB, were studied by the test of Indomethacin, Cl2Hg, Domperidone, Chlorpromazine and Acetazolamide, where each drug was given as pretreatment. Was conclude that TDB give gastric cytoprotection by the mechanism of the nonprotein sulfhydryl, by to be one peripheral agonist of the neuronal dopamine receptors, by increase of endogenous prostaglandin, by little increment of cAMP and no participate the gastric bicarbonate secretion.
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