Metabolic base production and mucosal vulnerability during acid inhibition in a mammalian stomach in vitro
Digestive Diseases and Sciences, ISSN: 0163-2116, Vol: 41, Issue: 5, Page: 964-971
1996
- 4Citations
- 1Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations4
- Citation Indexes4
- CrossRef2
- Captures1
- Readers1
Article Description
Acid inhibition increases gastric mucosal susceptibility to damage by luminal acid. This might be due to reduced metabolic CO and bicarbonate whereas, during normal acid, secretion cytoprotective CO/HCO production parallels acid production. Metabolic activity and mucosal damage caused by luminal acid perfusion was determined in an in vitro mouse stomach, with and without acid inhibition, and at 0%, 1%, or 5% serosal CO supply. Without acid inhibition there was no mucosal damage at any level of serosal CO/HCO supply. Acid inhibition reduced metabolic CO production by 29% (P < 0.004) and resulted in microscopic damage to 55% of the mucosal area and perforation in four of five stomachs (P < 0.05). Although, 1% CO supply completely replaced the reduction in metabolic CO, it did not protect against mucosal damage. Overreplacement by 5% serosal CO/HCO was required to prevent damage. There was no correlation between luminal CO/HCO output and mucosal damage. The protection by endogenous or exogenous CO/HCO appears to act intracellularly rather than by intragastric or intercellular neutralization.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0029926766&origin=inward; http://dx.doi.org/10.1007/bf02091538; http://www.ncbi.nlm.nih.gov/pubmed/8625770; http://link.springer.com/10.1007/BF02091538; http://www.springerlink.com/index/pdf/10.1007/BF02091538; http://www.springerlink.com/index/10.1007/BF02091538; https://dx.doi.org/10.1007/bf02091538; https://link.springer.com/article/10.1007/BF02091538
Springer Nature
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