Cytoprotective action of histamine against 0.6N HCl-induced gastric mucosal injury in rats; Comparative study with adaptive cytoprotection induced by exogenous acid.

Takeuchi, Koji; Nishiwaki, Hideyuki; Furukawa, Osamu; Okabe, Susumu

doi:10.1254/jjp.44.335

Cited by 16 publications

(7 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…isoprenaline and forskolin) makes it difficult to correlate the effect of indomethacin to changes in cyclic AMP levels inside the parietal cells. A possible release of PGs by histamine, recently suggested by some authors [2,7] was not confirmed in our study, since no differences were found in PGs levels in the mucosal fluid before and after histamine stimulation. The use of immature animals may perhaps explain the low levels of PGs produced; the experiments carried out with arachidonic acid tend to exclude the possibility that the low production of PGs was due to an insufficient amount of substrate for the action of cyclooxygenase.…”

Section: Discussioncontrasting

confidence: 85%

“…Recently a release of PGs by histamine has been observed in rats and the cytoprotective action of histamine in this species was ascribed to this effect [7]. The aim of the present study was to investigate the role of endogenous PGs in the secretory effect of histamine, by using different cyclooxygenase inhibitors and by measuring PGs production in the mucosal solution.…”

Section: Introductionmentioning

confidence: 95%

See 1 more Smart Citation

Effect of histamine on gastric acid secretion “in vitro”: Interference with endogenous prostaglandins

et al. 1990

View full text Add to dashboard Cite

The interference between histamine and endogenous prostaglandins (PGs) was investigated in the isolated gastric fundus from immature rats by evaluating the effect of nonsteroidal antiinflammatory agents (NSAIDs) on the acid response to histamine and the effect of histamine on PGs production by the gastric mucosa. Indomethacin (10(-5) M) and diclofenac (10(-5) M) caused a dose-dependent enhancement of the response to histamine, dimaprit and DBcAMP, but did not affect bethanechol-, isoprenaline- and forskolin-induced acid production. The enhancing effect of indomethacin was abolished in low Ca2+ medium. PGE2 and 6-keto PGF1 alpha levels in the mucosal solution were not modified by histamine, while being reduced by indomethacin. From these data it is concluded that endogenous PGs may negatively modulate the secretory response to histamine. However, a direct effect of the amine on cyclooxygenase to increase PGs synthesis seems to be excluded since histamine did not modify PGs levels in the mucosal solution.

show abstract

Section: Discussioncontrasting

confidence: 85%

Section: Introductionmentioning

confidence: 95%

Effect of histamine on gastric acid secretion “in vitro”: Interference with endogenous prostaglandins

et al. 1990

View full text Add to dashboard Cite

show abstract

“…Six hours after the administration of the test compounds, the animals were euthanized. Excised stomachs were inflated with and fixed by immersion in 2% formalin [24], Then they were opened along the greater curvature. After rinsing with 2% formalin, the mucosa was examined for the presence of erosion under a binocular micro scope.…”

Section: Irritative Action On Tlw Rat Stomachmentioning

confidence: 99%

Evaluation of Pharmacological Profile of Meloxicam as an Anti-Inflammatory Agent, with Particular Reference to Its Relative Selectivity for Cyclooxygenase-2 Over Cyclooxygenase-1

Ogino

Hatanaka²,

Kawamura³

et al. 1997

Pharmacology

View full text Add to dashboard Cite

We studied the anti-inflammatory activity of meloxicam on rat carrageenin-induced pleurisy and its toxicity for rat gastric mucosa, relative to its in vitro inhibitory potency against partially purified cyclooxygenase (COX)-1 and COX-2 preparations in order to clarify the pharmacological profile of the compound as an anti-inflammatory agent. In rat carrageenin-induced pleurisy, the plasma exudation rate peaked at 5 h, at which time COX-2 was detectable in cells from the pleural exudate. Meloxicam and piroxicam (1 and 3 mg/kg) and NS-398 (3 mg/kg) showed almost equal anti-inflammatory potency against 5-hour pleurisy. A single oral administration of the compounds caused a dose-dependent increase in the number of rats with gastric mucosal erosion. The ED₅₀ value for meloxicam (5.92 mg/kg) was significantly higher than that for piroxicam (1.76 mg/kg), indicating that meloxicam is safer. Indometacin showed intermediate safety (2.59 mg/kg). In in vitro experiments, indometacin inhibited COX-1 about 1.7 times more potently than COX-2. NS-398 inhibited COX-2 with an IC50 of 0.32 µM, but never affected COX-1 activity, even at 100 µM. In the same assay system, meloxicam inhibited COX-2 about 12 times more selectively than COX-1. Piroxicam, however, inhibited both isoforms almost equally. These results indicate that meloxicam is a potent anti-inflammatory agent with low gastric toxicity. One reason for its in vivo pharmacological profile may be related to its relative selectivity for COX-2 over COX-1. Thus, meloxicam may belong to a group of COX-2 selective anti-inflammatory agents with a better safety profile than conventional COX-1 and COX-2 nonselective anti-inflammatory agents.

show abstract

“…The response caused by 100 mM HCl is mediated only by PGs, whereas that caused by 200 mM HCl is mediated by both capsaicin-sensitive afferent neurons and NO in addition to endogenous PGs. We previously examined the effect of HCl at various concentrations (0.1ϳ0.35 M) on transmucosal PD of rat stomachs and found that the PD was not decreased by HCl even at 0.25 M (27). Thus, it is likely that 200 mM HCl, unlike 0.5 M NaCl, does not damage surface epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Distinct mechanisms of acid-induced HCO₃⁻secretion in normal and slightly permeable stomachs

Aihara

Sasaki²,

Ise³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

Self Cite

View full text Add to dashboard Cite

. Distinct mechanisms of acidinduced HCO 3 Ϫ secretion in normal and slightly permeable stomachs. Am J Physiol Gastrointest Liver Physiol 291: G464 -G471, 2006. First published May 18, 2006 doi:10.1152/ajpgi.00048.2006.-We investigated the regulatory mechanism of acid-induced HCO 3 Ϫ secretion in the slightly permeable rat stomach after an exposure to hyperosmolar NaCl. Under urethane anesthesia, a rat stomach was mounted on a chamber and perfused with saline, and the secretion of HCO 3 Ϫ was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. Acidification of the normal stomach with 100 mM HCl increased HCO 3 Ϫ secretion, and this response was totally inhibited by pretreatment with indomethacin but not N G -nitro-L-arginine methyl ester (L-NAME) or chemical ablation of capsaicin-sensitive afferent neurons. Exposure of the stomach to 0.5 M NaCl deranged the unstirred mucus gel layer without damaging the surface epithelial cells. The stomach responded to 0.5 M NaCl by secreting slightly more HCO 3 Ϫ , in an indomethacin-inhibitable manner, and responded to even 10 mM HCl with a marked rise in HCO 3 Ϫ secretion, although 10 mM HCl did not have an effect in the normal stomach. The acid-induced HCO 3 Ϫ response in the NaCl-treated stomach was significantly but partially attenuated by indomethacin, L-NAME, or sensory deafferentation and was totally abolished when these treatments were combined. These results suggest that gastric HCO 3 Ϫ secretion in response to acid is regulated by two independent mechanisms, one mediated by prostaglandins (PGs) and the other by sensory neurons and nitric oxide (NO). The acid-induced HCO 3 Ϫ secretion in the normal stomach is totally mediated by endogenous PGs, but, when the stomach is made slightly permeable to acid, the response is markedly facilitated by sensory neurons and NO.gastric HCO 3 Ϫ secretion; mucosal acidification; capsaicin-sensitive afferent neurons; prostaglandin; nitric oxide; rat THE SECRETION of HCO 3 Ϫ plays a crucial role in the protection of the gastroduodenal mucosa from acid (5, 10). The secretion increases in response to mucosal acidification, and the process is mediated by multiple factors, including endogenous prostaglandins (PGs) and nitric oxide (NO) as well as neuronal pathways (12,22,29,30). Recently, we found that the mechanism underlying acid-induced HCO 3 Ϫ secretion in the stomach differed depending on the concentration of acid; the response caused by 100 mM HCl was mediated only by PGs, whereas that caused by 200 mM HCl was mediated by both capsaicinsensitive afferent neurons and NO in addition to PGs (1). It is assumed that 100 mM HCl applied topically to the stomach increases PG biosynthesis by itself but does not acidify the mucosa enough to activate afferent neurons, resulting in an increase of HCO 3 Ϫ secretion that is totally dependent on endogenous PGs but not afferent neurons or NO.Mucus adherent to the luminal surface of the mucosa provides a zone of low turbulence (unstirred layer), allowing the development of a gradient f...

show abstract

Cytoprotective action of histamine against 0.6N HCl-induced gastric mucosal injury in rats; Comparative study with adaptive cytoprotection induced by exogenous acid.

Cited by 16 publications

References 16 publications

Effect of histamine on gastric acid secretion “in vitro”: Interference with endogenous prostaglandins

Effect of histamine on gastric acid secretion “in vitro”: Interference with endogenous prostaglandins

Evaluation of Pharmacological Profile of Meloxicam as an Anti-Inflammatory Agent, with Particular Reference to Its Relative Selectivity for Cyclooxygenase-2 Over Cyclooxygenase-1

Distinct mechanisms of acid-induced HCO₃⁻secretion in normal and slightly permeable stomachs

Contact Info

Product

Resources

About

Cytoprotective action of histamine against 0.6N HCl-induced gastric mucosal injury in rats; Comparative study with adaptive cytoprotection induced by exogenous acid.

Cited by 16 publications

References 16 publications

Effect of histamine on gastric acid secretion “in vitro”: Interference with endogenous prostaglandins

Effect of histamine on gastric acid secretion “in vitro”: Interference with endogenous prostaglandins

Evaluation of Pharmacological Profile of Meloxicam as an Anti-Inflammatory Agent, with Particular Reference to Its Relative Selectivity for Cyclooxygenase-2 Over Cyclooxygenase-1

Distinct mechanisms of acid-induced HCO3−secretion in normal and slightly permeable stomachs

Contact Info

Product

Resources

About

Distinct mechanisms of acid-induced HCO₃⁻secretion in normal and slightly permeable stomachs