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Effect of omeprazole on sodium and potassium output in pentagastrin-stimulated equine gastric contents.

Abstract: To better characterize the source of the large nonparietal secretory response to pentagastrin (PG) expressed in gastric contents of cannulated horses. Methods: Adult cross-bred horses: 4 geldings and 1 mare. Methods: Horses were prepared by surgical insertion of a silastic gastric cannula from which gastric contents after feed was withheld could be continuously collected by gravity drainage. During experiments, the horses were lightly restrained in stocks, the gastric cannula was opened, and a catheter was inserted into a jugular vein. Over the next 5 hours, gastric contents were collected in 15-minute aliquots for which volume, pH, [Na+], and [K+] were measured. During the first hour, treatment was not administered. At the start of the second hour, either 0.5 mg of omeprazole (OME; dissolved in glycerol formal)/kg of body weight, or 0.9% NaCl (PSS) of comparable volume, was given IV at random as a bolus. At the start of the third hour, IV infusion of PG (6 micrograms/ kg/h) was started and continued for the next 2 hours. Results: The response to PG in the PSS-treated horses was similar to that previously seen-significant decrease in pH and increase in volume of gastric contents, and no change in [K+] and [Na+], but a modest volume-related increase in their respective outputs. After OME treatment, pH of the contents increased sharply and remained between 5 and 6 throughout PG infusion. Sodium concentration significantly increased after OME and virtually paralleled the pH response throughout the rest of the experiment; volume of gastric contents significantly increased in response to PG infusion and resulted in a significant increase in Na output. There was no change in K output in OME-treated animals. Conclusions: PG induces a marked, nonparietal, secretory response into the gastric contents of cannulated horses. The volume and [Na+] of this response was maintained after pretreatment with OME, although the pH of the contents became basic, indicating that this nonparietal response is not mediated by an OME-sensitive proton pump.
Publication Date: 1996-11-01 PubMed ID: 8915445
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  • Journal Article

Summary

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The research study investigates the impact of the drug omeprazole on the output of sodium and potassium in gastric contents of horses stimulated by pentagastrin. The results demonstrate that while sodium levels increased significantly post-omeprazole treatment, potassium levels remained unchanged.

Research Methodology

  • The study was conducted on adult cross-bred horses (4 geldings and 1 mare) that underwent surgery for the insertion of a gastric cannula, which enables researchers to collect gastric contents continuously by gravity drainage.
  • In the experiment setup, the horses were lightly restrained in stocks, the gastric cannula was opened, and a catheter was inserted into the horse’s jugular vein.
  • Over a period of 5 hours, gastric content was collected every 15 minutes to measure its volume, pH, and concentration of sodium ([Na+]) and potassium ([K+]).
  • During the experiment’s first hour, no treatment was administered.
  • At the start of the second hour, either 0.5 mg of omeprazole per kg of body weight or a comparable volume of 0.9% sodium chloride solution was administered intravenously as a random bolus.
  • A continuous intravenous infusion of pentagastrin started from the beginning of the third hour and lasted for two hours.

Research Findings

  • The response to pentagastrin in horses treated with sodium chloride was consistent with prior studies—there was a significant decrease in pH and an increase in the volume of gastric contents.
  • Sodium and potassium concentrations remained unchanged, while their respective outputs showed a minor increase that corresponded with the volume.
  • Post-omeprazole treatment, the pH of the gastric contents increased substantially and stayed between 5 and 6 throughout pentagastrin infusion.
  • The sodium concentration showed a significant rise after omeprazole treatment, closely mirroring the pH response for the rest of the experiment.
  • The gastric content volume grew significantly in response to pentagastrin infusion, leading to a notable surge in sodium output.
  • However, there was no change observed in potassium output after omeprazole treatment.

Conclusion

  • Pentagastrin significantly stimulates a nonparietal secretory response in the gastric contents of cannulated horses.
  • Despite pretreatment with omeprazole, the volume and sodium concentration of this response was maintained.
  • The pH content became more basic, indicating that the nonparietal response isn’t mediated by an omeprazole-sensitive proton pump.

Cite This Article

APA
Merritt AM, Burrow JA, Horbal MJ, Madison JB, Tran T. (1996). Effect of omeprazole on sodium and potassium output in pentagastrin-stimulated equine gastric contents. Am J Vet Res, 57(11), 1640-1644.

Publication

ISSN: 0002-9645
NlmUniqueID: 0375011
Country: United States
Language: English
Volume: 57
Issue: 11
Pages: 1640-1644

Researcher Affiliations

Merritt, A M
  • Island Whirl Equine Colic Research Laboratory, Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville 32610-013, USA.
Burrow, J A
    Horbal, M J
      Madison, J B
        Tran, T

          MeSH Terms

          • Animals
          • Anti-Ulcer Agents / pharmacology
          • Female
          • Gastric Juice / chemistry
          • Gastric Juice / drug effects
          • Gastric Mucosa / metabolism
          • Horses / physiology
          • Male
          • Omeprazole / pharmacology
          • Pentagastrin / pharmacology
          • Potassium / analysis
          • Sodium / analysis
          • Stomach / drug effects

          Citations

          This article has been cited 1 times.
          1. Crothers JM Jr, Forte JG, Machen TE. Computer modeling of gastric parietal cell: significance of canalicular space, gland lumen, and variable canalicular [K+]. Am J Physiol Gastrointest Liver Physiol 2016 May 1;310(9):G671-81.
            doi: 10.1152/ajpgi.00431.2015pubmed: 26847387google scholar: lookup