Alkaline tide: Difference between revisions
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[[Postprandial]] (i.e., after a meal) alkaline tide lasts until the acids in food absorbed in the small intestine reunite with the bicarbonate that was produced when the food was in the stomach. Thus, alkaline tide is self-limited and normally lasts less than two hours. |
[[Postprandial]] (i.e., after a meal) alkaline tide lasts until the acids in food absorbed in the small intestine reunite with the bicarbonate that was produced when the food was in the stomach. Thus, alkaline tide is self-limited and normally lasts less than two hours. |
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Postprandial alkaline tide has also been shown to be a causative agent of [[calcium oxalate]] [[urolithiasis|urinary stones]] in cats,<ref> |
Postprandial alkaline tide has also been shown to be a causative agent of [[calcium oxalate]] [[urolithiasis|urinary stones]] in cats,<ref>{{cite journal |first=DF |last=Taton |last2=Hamar |first2=D |last3=Lewis |first3=LD |title=Evaluation of ammonium chloride as a urinary acidifier in the cat |journal=[[Journal of the American Veterinary Medical Association]] |date=15 February 1984 |volume=184 |page=433–436 }}</ref> and potentially in other species.<ref>McGavin, MD., Zachary, JF. ''Pathologic Basis of Veterinary Disease, Fourth Edition, Mosby, 2007, pp. 680–686.''</ref> |
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A more pronounced alkaline tide results from [[vomiting]], which stimulates hyperactivity of gastric [[parietal cell]]s to replace lost stomach acid.{{verification needed|date=August 2015}} Thus, protracted vomiting can result in [[metabolic alkalosis]].<ref name="nature">{{cite journal|url=http://www.nature.com/ki/journal/v1/n5/abs/ki197243a.html|title= The generation and maintenance of metabolic alkalosis|accessdate=2014-07-11|volume=1|doi=10.1038/ki.1972.43|journal=Kidney International|pages=306–321}}</ref> |
A more pronounced alkaline tide results from [[vomiting]], which stimulates hyperactivity of gastric [[parietal cell]]s to replace lost stomach acid.{{verification needed|date=August 2015}} Thus, protracted vomiting can result in [[metabolic alkalosis]].<ref name="nature">{{cite journal|url=http://www.nature.com/ki/journal/v1/n5/abs/ki197243a.html|title= The generation and maintenance of metabolic alkalosis|accessdate=2014-07-11|volume=1|doi=10.1038/ki.1972.43|journal=Kidney International|pages=306–321}}</ref> |
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Revision as of 22:35, 12 February 2019
Alkaline tide refers to a condition, normally encountered after eating a meal, where during the production of hydrochloric acid by parietal cells in the stomach, the parietal cells secrete bicarbonate ions across their basolateral membranes and into the blood, causing a temporary increase in pH.[1]
During hydrochloric acid secretion in the stomach, the gastric parietal cells extract chloride anions, carbon dioxide, water and sodium cations from the blood plasma and in turn release bicarbonate back into the plasma after forming it from carbon dioxide and water constituents. This is to maintain the plasma's electrical balance, as the chloride anions have been extracted. The bicarbonate content causes the venous blood leaving the stomach to be more alkaline than the arterial blood delivered to it.
The alkaline tide is neutralised by a secretion of H+ into the blood during HCO3− secretion in the pancreas.[2]
Postprandial (i.e., after a meal) alkaline tide lasts until the acids in food absorbed in the small intestine reunite with the bicarbonate that was produced when the food was in the stomach. Thus, alkaline tide is self-limited and normally lasts less than two hours.
Postprandial alkaline tide has also been shown to be a causative agent of calcium oxalate urinary stones in cats,[3] and potentially in other species.[4]
A more pronounced alkaline tide results from vomiting, which stimulates hyperactivity of gastric parietal cells to replace lost stomach acid.[verification needed] Thus, protracted vomiting can result in metabolic alkalosis.[5]
References
 | This article includes a list of general references, but it lacks sufficient corresponding inline citations. (July 2010) |
- ^ Margaret E. Smith; Dion G. Morton (18 November 2011). The Digestive System: Systems of the Body Series. Elsevier Health Sciences UK. p. 52. ISBN 978-0-7020-4841-8.
- ^ Margaret E. Smith; Dion G. Morton (18 November 2011). The Digestive System: Systems of the Body Series. Elsevier Health Sciences UK. p. 85. ISBN 978-0-7020-4841-8.
- ^ Taton, DF; Hamar, D; Lewis, LD (15 February 1984). "Evaluation of ammonium chloride as a urinary acidifier in the cat". Journal of the American Veterinary Medical Association. 184: 433–436.
- ^ McGavin, MD., Zachary, JF. Pathologic Basis of Veterinary Disease, Fourth Edition, Mosby, 2007, pp. 680–686.
- ^ "The generation and maintenance of metabolic alkalosis". Kidney International. 1: 306–321. doi:10.1038/ki.1972.43. Retrieved 2014-07-11.
- Gennari, F. John (2005). Acid-base disorders and their treatment. Informa Health Care. p. 217. ISBN 0-8247-5915-X.
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