Measurement of bicarbonate output from the intact human oesophagus.

Brown, Charles E.; Snowdon, Claire; Slee, B.; Sandle, L. N.; Rees, W. D. W.

doi:10.1136/gut.34.7.872

Cited by 30 publications

(22 citation statements)

References 23 publications

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“…Because of the minimal amount of bicarbonate and the fact that most unrelated peaks occur during the evening/night, this seems an unlikely explanation. In the esophagus, the median secretion of bicarbonate ranges from 160 to 490 mmol h (1 10 cm (1 , no data on circadian rhythm of this production exist [24,25]. The peaks in-between meals are also unlikely to be explained by production of bicarbonate by the esophagus.…”

Section: Discussionmentioning

confidence: 96%

Effect of various test meals on gastric and jejunal carbon dioxide: A study in healthy subjects

Mensink

Geelkerken²,

Huisman

et al. 2006

Scandinavian Journal of Gastroenterology

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Section: Discussionmentioning

confidence: 96%

Effect of various test meals on gastric and jejunal carbon dioxide: A study in healthy subjects

Mensink

Geelkerken²,

Huisman

et al. 2006

Scandinavian Journal of Gastroenterology

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“…Bicarbonate derived from saliva and esophageal submucosal glands has been demonstrated to protect against acidic gastric refluxate (Brown et al, 1993(Brown et al, ,1995Helm et al, 1987). Tobey et al (1989), using rabbit esophagus in an Ussing chamber, showed that intercellular bicarbonate ions from adventitial perfusion protected the epithelium from acid injury, which was assessed histologically and by decline in voltage and electrical resistance measured across the esophageal mucosa.…”

Section: Discussionmentioning

confidence: 99%

Carbonic Anhydrase Isoenzymes I, II, III, and IV Are Present in Human Esophageal Epithelium

Christie

Thomson

Xue

et al. 1997

J Histochem Cytochem.

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Carbonic anhydrase (CA) isoenzymes have been widely studied in the gastrointestinal tract, where they mediate membrane transport events and pH regulation. However, the esophagus has generally received scant attention. In an immunohistochemical study confirmed by Western blotting, we have detected four CA isoenzymes (CAI, II, III, and IV) in the epithelium of human esophagus. Isoenzymes I, III, and sometimes IV (<10%) were present in the cytoplasm of basal cells and II and IV in the cytoplasm and cell surface membranes, respectively, of suprabasal cells (prickle cells). The localization of CAIV to the plasma membranes was confirmed by electron microscopic immunocytochemistry. CA was effectively divided at the basal-suprabasal interface between low-activity CAI and III (basal) and high-activity CAII and IV (suprabasal). Carbonic anhydrase in esophageal epithelial cells may have several functions: elimination of CO2 and metabolites, participation in membrane transport events during active cell growth, and pH regulation as a protective mechanism against acidic gastric reflux.

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confidence: 99%

“…In humans, esophageal SMG have the capacity to secrete HCO 3 Ϫ in amounts sufficient to neutralize residual volumes of acid left in the esophagus after bolus clearance (28). Quantitatively, this HCO 3Ϫ secretion can approach the HCO 3 Ϫ output of salivary glands at rest (10,21,27,28).Although potentially of clinical importance, there is little information about the cellular mechanisms by which esophageal SMG secrete HCO 3Ϫ . This is because of the technical difficulties of isolating the human esophagus from salivary and gastric contamination for the accurate collection and quantitation of SMG HCO 3…”

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confidence: 99%

HCO₃⁻secretion in the esophageal submucosal glands

Abdulnour‐Nakhoul¹,

Nakhoul²,

Wheeler³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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The mammalian esophagus has the capacity to secrete a HCO(3)(-) and mucin-rich fluid in the esophageal lumen. These secretions originate from the submucosal glands (SMG) and can contribute to esophageal protection against refluxed gastric acid. The cellular mechanisms by which glandular cells achieve these secretions are largely unknown. To study this phenomenon, we used the pH-stat technique to measure luminal alkali secretion in an isolated, perfused pig esophagus preparation. Immunohistochemistry was used to localize receptors and transporters involved in HCO(3)(-) transport. The SMG-bearing esophagus was found to have significant basal alkali secretion, predominantly HCO(3)(-), which averaged 0.21 +/- 0.04 microeq.h(-1).cm(-2). This basal secretion was doubled when stimulated by carbachol but abolished by HCO(3)(-) or Cl(-) removal. Basal- and carbachol-stimulated secretions were also blocked by serosal application of atropine, pirenzipine, DIDS, methazolamide, and ethoxzolamide. The membrane-impermeable carbonic anhydrase inhibitor benzolamide, applied to the serosal bath, partially inhibited basal HCO(3)(-) secretion and blocked the stimulation by carbachol. Immunohistochemistry using antibodies to M(1) cholinergic receptor or carbonic anhydrase-II enzyme showed intense labeling of duct cells and serous demilunes but no labeling of mucous cells. Labeling with an antibody to Na(+)-(HCO(3)(-))(n) (rat kidney NBC) was positive in ducts and serous cells, whereas labeling for Cl(-)/HCO(3)(-) exchanger (AE2) was positive in duct cells but less pronounced in serous cells. These data indicate that duct cells and serous demilunes of SMG play a role in HCO(3)(-) secretion, a process that involves M(1) cholinergic receptor stimulation. HCO(3)(-) transport in these cells is dependent on cytosolic and serosal membrane-bound carbonic anhydrase. HCO(3)(-) secretion is also dependent on serosal Cl(-) and is mediated by DIDS-sensitive transporters, possibly NBC and AE2.

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Measurement of bicarbonate output from the intact human oesophagus.

Abstract: Injury of the oesophageal mucosa can result from exposure to refluxed gastric acid and pepsin. Competence

Cited by 30 publications

References 23 publications

Effect of various test meals on gastric and jejunal carbon dioxide: A study in healthy subjects

Effect of various test meals on gastric and jejunal carbon dioxide: A study in healthy subjects

Carbonic Anhydrase Isoenzymes I, II, III, and IV Are Present in Human Esophageal Epithelium

HCO₃⁻secretion in the esophageal submucosal glands

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Measurement of bicarbonate output from the intact human oesophagus.

Abstract: Injury of the oesophageal mucosa can result from exposure to refluxed gastric acid and pepsin. Competence

Cited by 30 publications

References 23 publications

Effect of various test meals on gastric and jejunal carbon dioxide: A study in healthy subjects

Effect of various test meals on gastric and jejunal carbon dioxide: A study in healthy subjects

Carbonic Anhydrase Isoenzymes I, II, III, and IV Are Present in Human Esophageal Epithelium

HCO3−secretion in the esophageal submucosal glands

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HCO₃⁻secretion in the esophageal submucosal glands