Effect of aminoguanidine, chlorpromazine and NSD‐1055 on gastric secretion and ulceration in the Shay rat

Radwan, A. G.; West, G. B.

doi:10.1111/j.1476-5381.1971.tb09946.x

Cited by 6 publications

(5 citation statements)

References 15 publications

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“…With regard to pharmacological experiments, though some authors have reported that HDI inhibit gastric acid secretion in the rat [20][21][22][23] others could not confirm it [24][25][26][27]. In our experiments, HDI did not inhibit the pentagastrin-stimulated gastric acid secretion in the doses applied, but these compounds markedly potentiated and also prolonged the antisecretory effect of histamine H2-receptor antagonists in both pre-and simultaneous treatments.…”

Section: Discussioncontrasting

confidence: 70%

Induction of gastric histamine synthesis by H2-receptor antagonists: Potentiation of their antisecretory activity by histidine decarboxylase inhibitors

Huszti¹,

Pik

Frenkl

1980

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The activation of histamine (HA) formation in rat stomach was measured after repeated administration of histamine H2-receptor antagonists and the potentiation of their antisecretory activity was examined in histidine decarboxylase inhibitor (HDI)-pretreated rats. 40 mg/kg of metiamide, given intraperitoneally (i.p.) 24, 16 and 2 h prior to the examination, produced approximately 50% increase in the amount of 14C-histamine, formed from 14C-histidine in the stomach, and an almost equal enhancement in the gastric histidine decarboxylase (HD) activity. An equal dose of the compound did not influence the endogenous histamine level in the glandular stomach whereas it caused a significant increase in the serum histamine content. By similar treatment, 10 mg/kg of cimetidine enhanced the newly formed histamine in the rat stomach by 57%. The potent HDI, 2-hydroxy-5-carbomethoxy-benzyloxyamine (GYKI-11 121) suppressed the metiamide- and cimetidine-induced increases in histamine synthesis to slightly above or below the control values. In pharmacological studies, the antisecretory activity of histamine H2-receptor blockers could markedly be potentiated by HDI. In GYKI-11 121 and NSD-1055-pretreated rats, the inhibiting potency of metiamide and cimetidine on pentagastrin-stimulated gastric acid secretion, increased to approximately twice that of the original effect. Neither GYKI-11 121 nor NSD-1055 produced significant inhibition on pentagastrin-stimulated gastric acid secretion in the applied doses. These findings provided evidence for the feedback stimulation of gastric HA synthesis by H2-receptor blockers and confirmed the role of HA in the gastric acid secretion. Potentiation of the antisecretory activity of H2-receptor antagonists by HDI would be useful in the therapeutic application of these compounds.

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Section: Discussioncontrasting

confidence: 70%

Induction of gastric histamine synthesis by H2-receptor antagonists: Potentiation of their antisecretory activity by histidine decarboxylase inhibitors

Huszti¹,

Pik

Frenkl

1980

Agents and Actions

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“…Estimation of oxidative stress biomarkers in serum and gastric tissue Blood samples were collected in centrifuge tubes then allow clotting for serum separation. Centrifugation at 3000 rpm for 15 minutes induced clear non-hemolysed sera that used for antioxidants activity assay: catalase (CAT) [24] , superoxide dismutase (SOD) [25] as well as determination of malondialdehyde (MDA) level concentrations [26] .…”

Section: Evaluation Of Fundic Mucosal Injurymentioning

confidence: 99%

Histological and Biochemical Study on the Estrogen Role in Indomethacin-induced Gastric Ulcer of Menopausal Rats

Mohamed

Ahmed

Shalaby

et al. 2019

Journal of Medical Histology

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Background: Estrogen is a principal female sex hormone that originally characterized by its importance in sexual growth and reproduction. Nevertheless, emergent evidence proposes clinical relationship between estrogen/ estrogen receptors and gastric diseases. This association is definitely under several investigated topics. Aim: The current study designed to explore exogenous estrogen effect on indomethacin-induced gastric ulcers in postmenopausal female rats. Matrial and methods: Twenty-four female rats (200 ± 20 gram BW) were allocated randomly into four groups; control, ulcer-induced, ranitidine-treated and (ranitidine&estradiol velerate) combined-treated group. Animal in all group except control subjected to ovariectomy to assimilate menopausal condition. At end of the experiment, the stomach fundus examined macroscopically to assess the ulcer severity and ulcer score in different groups. Histopatholgical and biochemical evaluation also were performed and all results were statistically analyzed. Results: Indomethacin-induced gastric ulcer in ovariectomized rats showed destroyed fundic mucosa and mucus layer, increase oxidative stress markers, inflammatory mediators and myeloperoxidase. Treatment with ranitidine attenuated the histological and biochemical changes but within limits. Better improvement was accomplished when ranitidine combined with estrogen. Conclusion: The postmenopausal women should be supplemented with estrogen not only to control menopausal symptoms but also to protect and maintain gastric mucosal integrity.

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“…In rats with chronic gastric fistulae, NSD 1055 reduced the response to pentagas trin. Radwan and West (121) found that 200 mg/kg NSD 1055 intraperitoneally resulted in only a small reduction in the volume and total acidity of 16-hour Shay rats, but considerably reduced the incidence and extent of gastric ulcera tion. Becker and Sewing (14), using the anaesthetized gastric perfused rat, were only able to show inhibition of tetragastrin-stimulated gastric acid secretion with 100 mg/kg NSD 1055 when administered intravenously; when oral or intraperitoneal routes were used, tetragastrin-stimulated gastric acid secretion was poten tiated.…”

Section: Gastric Secretory Effects O F Decarboxylase Inhibitorsmentioning

confidence: 99%

Amino Acid Decarboxylase Enzymes – Vital or Irrelevant to Gastric Secretion?

Henman¹

1975

Digestion

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The location and discovery of histidine decarboxylase and aromatic L-amino acid decarboxylase in the stomach are described. Feeding and gastrin-like agents stimulate increased gastric histidine decarboxylase (HD) activity in rats. Procedures which result in increased gastrin release – often by raising antral pH – also have this action in intact but not in antrectomised rats. Evidence for a histaminic feedback mechanism controlling HD levels is discussed. HD activity is reduced by protein synthesis inhibitors and by chronic pyridoxine deficiency. The effects of inhibitors of HD on gastric secretion in rat, dog and man are reviewed. The role of HD and histamine in gastric secretion is considered.

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Effect of aminoguanidine, chlorpromazine and NSD‐1055 on gastric secretion and ulceration in the Shay rat

Cited by 6 publications

References 15 publications

Induction of gastric histamine synthesis by H2-receptor antagonists: Potentiation of their antisecretory activity by histidine decarboxylase inhibitors

Induction of gastric histamine synthesis by H2-receptor antagonists: Potentiation of their antisecretory activity by histidine decarboxylase inhibitors

Histological and Biochemical Study on the Estrogen Role in Indomethacin-induced Gastric Ulcer of Menopausal Rats

Amino Acid Decarboxylase Enzymes – Vital or Irrelevant to Gastric Secretion?

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