Disease relevance of epirizole

• In contrast, L-365, 260 (30 mg/kg) tended to reduce the severity of mepirizole-induced duodenal ulcers, with a slight inhibition of acid secretion, but it caused no influence on the healing response of these ulcers [1].
• Gastric acid secretion in the pylorus-ligated or acute fistula preparation was not affected by 10 mg/kg of mepirizole [2].
• Indomethacin (10 mg/kg subcutaneously) produced gastric ulcers, whereas mepirizole (100 mg/kg subcutaneously) produced exclusively duodenal ulcers [3].
• We studied the effect of tobacco cigarette smoke on the hyperemia at the margin of mepirizole-induced duodenal ulcer [4].
• The inhibitory activity of gastrointestinal lesions by mepirizole was in proportion to the activities that antagonized the shortening of the small intestine, loss of body weight and delay of charcoal transport by indomethacin [5].

High impact information on epirizole

• After subcutaneous administration of 200 mg/kg of mepirizole, basal gastric acid secretion remained unchanged for 5 h but duodenal alkaline output, reliably measured, decreased significantly (p less than 0.05) within 2 h [6].
• Intravenous secretin (1 CU/kg X h) had no effect on duodenal alkaline secretion in either saline- (154 mM NaCl) or mepirizole-treated animals [6].
• On the other hand, a duodenal ulcerogen, mepirizole (200 mg/kg, s.c. ) caused an increase in acid secretion and resulted in penetrating ulcers in the proximal duodenum, and these ulcers gradually healed over 3 weeks [1].
• Study of the modifications caused by cisplatin, transplatin, and Pd(II) and Pt(II) mepirizole derivatives on pBR322 DNA by atomic force microscopy [7].
• Animals were given mepirizole (200 mg/kg, s.c.) for induction of duodenal ulcers, and gastric acid and duodenal HCO3- secretions were measured with or without pretreatment of PACAP-27 or VIP [8].

Chemical compound and disease context of epirizole

• On the basis of ED50 values, YM022 was 5 times less potent than famotidine and as potent as omeprazole against mepirizole-induced duodenal ulcers [9].
• FRG-8701 showed antiulcer activity against stress and indomethacin gastric ulcer and mepirizole duodenal ulcer [10].
• The development of duodenal ulcers and gastric erosions caused by mepirizole was also potently inhibited by omeprazole at 3-10 mg/kg given orally [11].
• Prostaglandin deficiency by itself is not the cause of mepirizole-induced duodenal ulcers in rats [3].
• Role of accumulated gastric content in the pathogenesis of cysteamine- and mepirizole-induced duodenal ulcers in the rat [12].

Biological context of epirizole

• Acid secretory and duodenal ulcerogenic responses induced by mepirizole in anesthetized rats. Relation to body temperature [13].
• Role of active oxygen species and lipid peroxidation in mepirizole-induced duodenal ulcers in rats [14].
• Acute administration of cysteamine, MPTP, or mepirizole significantly delayed gastric emptying of the meal [15].
• [Mechanism of biological actions of mepirizole, a nonsteroidal anti-inflammatory agent. (I). Suppressive effects on the leukocytes chemotaxis in vivo and in vitro] [16].

Anatomical context of epirizole

• 16,16-Dimethyl prostaglandin E2 (dmPGE2, 30 micrograms/kg) administered s.c. significantly protected the duodenal mucosa against mepirizole-induced damage for up to 6 hr [17].
• These results suggest that the mechanism underlying mepirizole protection relates to both endogenous prostaglandins and sulfhydryl compounds present in the gastric mucosa, but does not relate to an inhibition of gastric motility [2].
• Mepirizole (60 and 200 mg/kg) administered s.c. induced damage in the surface epithelial cells of the rat proximal duodenum as early as 2 hr after the treatment [17].
• The stomachs of fasted guinea pigs given 200 mg/kg of mepirizole had superficial erosions at a high incidence (93.3%) [18].
• Pretreatment with NC-1300 dose-dependently protected the gastric mucosa from damage induced by pylorus ligation, water-immersion stress, aspirin, and indomethacin, and the duodenal mucosa from damage induced by mepirizole in rats [19].

Associations of epirizole with other chemical compounds

• Pretreatment of rats with YJA20379-6 dose-dependently protected the gastric mucosa from damage induced by water-immersion stress, indomethacin and absolute ethanol, and the duodenal mucosa from damage induced by mepirizole [20].
• In contrast, VIP (8 nmol/kg, i.v.) given by bolus injection significantly decreased acid secretion induced by mepirizole, in addition to stimulation of HCO3- secretion, and prevented duodenal lesions in response to mepirizole [8].
• The role of body temperature in the acid stimulatory mechanism by mepirizole, a duodenal ulcerogen, was investigated in urethane-anesthetized rats [13].
• We investigated the HCO3- stimulatory mechanism of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in the anesthetized rat duodenum and examined whether L-NAME protects against mepirizole-induced duodenal damage [21].
• Augmentation of cysteamine and mepirizole-induced lesions in the rat duodenum and stomach by histamine or indomethacin [22].

Gene context of epirizole

• Antacids, anticholinergic agents, a histamine H2-receptor antagonist and 16-DMPGE2 dose-dependently inhibited mepirizole-induced duodenal ulcers [23].
• Twenty-four hours after rats were injected with an ulcerogenic dose of mepirizole, they were exposed to tobacco cigarette smoke and duodenal mucosal blood flow was measured by IAP autoradiography [4].
• Mepirizole at 200 mg/kg given intraduodenally significantly reduced the volume of gastric juice but increased the acidity and pepsin activity in both pylorus-ligated and acute fistula rats [18].
• In addition, both endothelin-1 and TY-10957 significantly prevented mepirizole-induced duodenal lesions at the doses that caused an increase of duodenal HCO3- secretion and a decrease of gastric acid secretion [24].

Analytical, diagnostic and therapeutic context of epirizole

• Oral administration of mepirizole (200 mg/kg) resulted in ulcer lesions in the proximal duodenum [14].
• Analytical studies on mepirizole and its metabolites. II. Identification of the human urinary metabolites of mepirizole with stable isotope labeling [25].

References