1,721,041 research outputs found
Famotidine Prevent Deep Histologic Lesion Induced by 0.6N HCl in Rat Gastric Mucosa : Role of Parietal Cells
No full textThe assessment of the protective actions of H-2-receptor antagonists against gastric mucosal Lesions by necrotizing agents relies on the gross observation of the gastric mucosa only. We examined the activity of famotidine against 0.6 N HCl-induced damage and the role of parietal cells by light and transmission electron microscopy. Rats received famotidine 0.3-10 mg/kg intragastrically. Sixty minutes later 0.6 N HCl (1 ml/rat) was given and after an additional 30 min the stomachs were removed. Macroscopically visible lesions were measured. Histologic lesions were scored on the basis of the depth. The ultrastructure of parietal cells in the isthmus-neck region was examined. Pretreatment with famotidine resulted in a slight increase of macroscopically visible gastric lesions in response to HCl. While the extent of total histologic damage was not modified, the antisecretory dose significantly reduced only lesions deep within the mucosa. Famotidine alone determined the dose-dependent occurrence of a distinct parietal cell morphological state, suggestive of inhibition of the secretory system. A causal link between the protective effect on the region where parietal cells are located, the percentage of cells shifting to the inhibited morphological state, and the inhibitory effect on acid secretion is proposed
(R)-alpha-methylhistamine inhibits ethanol-induced gastric lesions in the rat: involvement of histamine H3 receptors?
No full textThis study examined the gastroprotective effect of (R)-alpha-methylhistamine (MHA), a selective agonist of histamine H-3 receptors, Gastric lesions were induced in the rat by administering absolute ethanol in a volume of 1 ml. Stomachs were removed 1 h later and lesions evaluated both macroscopically and histologically. MHA dose-dependently inhibited ethanol-induced lesions in the range 1-100 mg/kg both by the intragastric and intraperitoneal route. Histological findings indicated that the number of mucous granules in surface and neck cells was increased and the process of reepithelialization was rapidly promoted by MHA. Thioperamide, at 10 mg/kg, inhibited the protective effect of 10 but not of 100 mg/kg of MHA. Larger doses of thioperamide could not be tested because of an interaction with ethanol causing central nervous system effects. Famotidine and indomethacin pretreatment only partially counteracted the MHA effect. The results indicate that MHA is highly effective in preventing ethanol-induced lesions but the exact mechanism is still uncertain
Effects of long-term (R)-alpha-methylhistamine administration on mucus-secreting and proliferative cells in the rat gastric mucosa
No full textComparison of the protective effect of (R)-alpha-methylhistamine and its prodrugs on gastric mucosal damage induced by ethanol in the rat
No full text1. The gastroprotective activity of two azomethine prodrugs of (R)-alpha-methylhistamine was examined in lesions induced by absolute ethanol (1 ml/rat intragastrically for 1 h).
2. Pretreatment with (R)-alpha-methylhistamine as well as with the prodrugs (30 and 100 mg/kg intragastrically [IG]) significantly reduced macroscopically visible lesions caused by ethanol, with protection being almost complete at 100 mg/kg.
3. Histologically, in rats pretreated with the three compounds ata dose of 100 mg/kg, the evidence of ; damage was rare, with the appearance of gastric mucosa being similar in the different treatment groups.
4. Present results are suggestive of a local component in the protective activity of (R)-alpha-methylhistamin
Appareil lymphatique périphérique absorbant (ALPA) et vaisseaux sanguins de l'appendice vermiforme: Aspects tridimensionnels et ultrastructuraux
No full textStimulation of gastric acid secretion by (R)-alpha-methylhistamine in the rat: influence of the increased gastric juice volume on ethanol-induced lesions.
No full textHistamine H3 receptors and the gastric mucosa: a link between protection and epithelial proliferation?
No full textThe role of histamine H3 receptors in the control of gastric functions is considered. The selective agonist of histamine H3 receptors, (R)-α-methylhistamine, reduces gastric damage exerted by mechanistically distinct noxious stimuli in the rat. Its effect is reversed by H3-receptor selective antagonists, ciproxifan and clobenpropit, while prevention of damage is similarly achieved with FUB 407, a reference compound for a novel class of histamine H3-receptor agonists structurally not related to histamine. It is concluded that H3 receptors are involved in the maintenance of gastric muscosal integrity. H3 receptors appear to have a minor role in the control of acid secretion, while they effectively enhance synthesis and secretion of mucus as well as increase the number of both surface mucous cells and mucous neck cells. H3 receptors ligands promptly increase the rate of proliferation in the gastric mucosa, their target being stem cells located in the isthmal region. They also influence the process of differentiation, by promoting the expansion of the lineage of surface mucous cells. Prevention of acute damage and regulation of cell cycle of gastric epithelial cells can be viewed as functionally linked effects, influenced by histamine H3 receptors
- …
