Effects of Omeprazole on Gastric Mucosal Blood Flow in the Conscious Rat

Mattsson, Hillevi; Larsson, Håkan

doi:10.3109/00365528708991496

Cited by 19 publications

(5 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As expected, the increase in GMBF response induced by histamine was closely associated with acid secretion; this response was almost completely attenuated when acid secretion was inhibited by cimetidine. These results are in agreement with findings of Mattsson and Larsson (1987), Kato et al (1993), and Pique et al (1992). It has been reported that enhanced acid secretion is induced by histamine in histidine decarboxylase (HDC)‐deficient mice.…”

Section: Discussionsupporting

confidence: 93%

Role of N‐methyl‐D‐aspartate receptors in gastric mucosal blood flow induced by histamine

Tsai

Lee

2004

J of Neuroscience Research

View full text Add to dashboard Cite

Ionotropic N-methyl-D-aspartate (NMDA) receptor agonists, L-aspartic acid (L-Asp) and NMDA, have been shown to inhibit histamine-stimulated acid secretion, but their effect on gastric mucosal blood flow (GMBF) is largely unknown. The aim of this study was to investigate whether L-Asp and NMDA inhibit histamine-stimulated GMBF and to examine the expression patterns of NMDA receptor subunits NR1, NR2A, and NR2B in rat stomach. Laser Doppler flowmetry was used to measure gastric blood flow in anesthetized rats. The GMBF was assessed during an intravenous infusion of histamine in the presence of tripelennamine. The effects of L-Asp and NMDA on histamine-induced gastric blood flow were examined. In addition, the distribution patterns of NR1-, NR2A-, and NR2B-contaning NMDA receptors in rat stomach were determined immunohistochemically by using specific antibodies against NR1, NR2A, and NR2B. Histamine-induced enhancement of GMBF depended on acid secretion and the activation of H(2)-receptors. Neither L-Asp nor NMDA had an effect on the spontaneous GMBF. However, L-Asp and NMDA reduced the histamine-induced increase in GMBF. DL-2-amino-5-phosphonopentanoic acid (AP-5), an NMDA receptor antagonist; and prazosin, an alpha(1)-receptor antagonist; but not propanolol, a beta(2)-receptor antagonist; or yohimbine, a alpha(2)-receptor antagonist; reversed the inhibitory effect of L-Asp and NMDA on the histamine-induced increase in GMBF. Therefore, L-Asp and NMDA inhibit histamine-induced GMBF via a mechanism involving the activation of NMDA receptors and alpha(1)- adrenoceptors. The fact that NMDA receptor subunits NR1, NR2A, and NR2B were found to be localized in the rat stomach as visualized immunohistochemically with specific antibodies against NR1, NR2A, and NR2B is consistent with this hypothesis.

show abstract

Section: Discussionsupporting

confidence: 93%

Role of N‐methyl‐D‐aspartate receptors in gastric mucosal blood flow induced by histamine

Tsai

Lee

2004

J of Neuroscience Research

View full text Add to dashboard Cite

show abstract

“…Variations in the transport rate of gastrin between the antral and corpus regions exert the strongest effect on acid levels (PRC coefficient ϭ 0.80, P Ͻ Ͻ 0.001). This is not unexpected given evidence for increased mucosal blood flow during feeding (49,69,79). We suggest that increasing blood flow increases the availability of gastrin in the corpus, thereby enhancing acid release.…”

Section: Importance Of Neural-independent Parameterssupporting

confidence: 61%

A model for integrative study of human gastric acid secretion

Joseph¹,

Zavros

Merchant

et al. 2003

Journal of Applied Physiology

View full text Add to dashboard Cite

We have developed a unique virtual human model of gastric acid secretion and its regulation in which food provides a driving force. Food stimulus triggers neural activity in central and enteric nervous systems and G cells to release gastrin, a critical stimulatory hormone. Gastrin stimulates enterochromaffin-like cells to release histamine, which, together with acetylcholine, stimulates acid secretion from parietal cells. Secretion of somatostatin from antral and corpus D cells comprises a negative-feedback loop. We demonstrate that although acid levels are most sensitive to food and nervous system inputs, somatostatin-associated interactions are also important in governing acidity. The importance of gastrin in acid secretion is greatest at the level of transport between the antral and corpus regions. Our model can be applied to study conditions that are not yet experimentally reproducible. For example, we are able to preferentially deplete antral or corpus somatostatin. Depletion of antral somatostatin exhibits a more significant elevation of acid release than depletion of corpus somatostatin. This increase in acid release is likely due to elevated gastrin levels. Prolonged hypergastrinemia has significant effects in the long term (5 days) by promoting enterochromaffin-like cell overgrowth. Our results may be useful in the design of therapeutic strategies for acid secretory dysfunctions such as hyper- and hypochlorhydria.

show abstract

“…Previous investigations showed that om eprazole did not significantly affect gastric prostaglandin synthesis [5,24], bicarbonate secretion [10], or mucosal blood flow [11,12]. A possible involvement of gastric mucus barrier has been hypothesized [8], but not yet dem onstrated.…”

Section: Correlation Analysismentioning

confidence: 99%

“…In addition, omeprazole was shown not to significantly affect bicarbonate secretion [10] or gastric mucosal blood flow [11,12].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Protection by Omeprazole against Experimental Gastric Mucosal Damage in Rats

et al. 1995

View full text Add to dashboard Cite

In the present study, the protective effect of omeprazole on gastric mucosa injury induced by ethanol •HCl in rats and the putative mechanisms involved in this action were investigated. Misoprostol and ranitidine were used as reference drugs. The morphometric analysis of histological sections showed that omeprazole caused a significant reduction of mucosal necrotic damage, this effect being associated with a marked increase in Alcian blue recovery from gastric bound mucus. In addition, omeprazole elicited a significant inhibition of gastric acid secretion from pylorus-ligated rats. Misoprostol exerted similar effects to those obtained with omeprazole, even if the Alcian blue recovery and the acid output were affected to a lesser extent. By contrast, ranitidine failed to influence both the mucosal damage and the Alcian blue recovery, while it exerted a marked inhibition on acid secretion. The present results indicate that omeprazole is effective in protecting gastric mucosa from necrotic damage induced by ethanol •HCl and suggest that an enhancement of gastric mucus barrier may account for this protective action.

show abstract

Effects of Omeprazole on Gastric Mucosal Blood Flow in the Conscious Rat

Cited by 19 publications

References 31 publications

Role of N‐methyl‐D‐aspartate receptors in gastric mucosal blood flow induced by histamine

Role of N‐methyl‐D‐aspartate receptors in gastric mucosal blood flow induced by histamine

A model for integrative study of human gastric acid secretion

Mechanisms of Protection by Omeprazole against Experimental Gastric Mucosal Damage in Rats

Contact Info

Product

Resources

About