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Some duodenal functions and their dependence on luminal NaCl
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
Manuscript (Other academic)
URN: urn:nbn:se:uu:diva-95371OAI: oai:DiVA.org:uu-95371DiVA: diva2:169554
Available from: 2007-01-12 Created: 2007-01-12 Last updated: 2014-04-07Bibliographically approved
In thesis
1. Luminal Hypotonicity and Duodenal Functions: An Experimental Study in the Rat
Open this publication in new window or tab >>Luminal Hypotonicity and Duodenal Functions: An Experimental Study in the Rat
2007 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

After drinking water, the fluid quickly leaves the stomach thereby creating a hypotonic luminal environment in the duodenum. This in turn constitutes a potential threat to the integrity of the duodenal epithelium. It therefore seems highly likely that luminal hypotonicity activates physiological mechanisms that aim to increase luminal osmolality. One such physiological mechanism may be to increase mucosal permeability thereby facilitating the transport of osmolytes into the lumen.

A draw-back of performing experiments in anesthetized animals is that surgery per se depresses gut functions, such as peristalsis, by mechanisms involving endogenous prostaglandins. In this thesis it is shown that inhibition of cyclooxygenase-2 (COX-2), in animals subjected to an abdominal operation, restore and/or improve duodenal functions such as motility, mucosal bicarbonate secretion, hypotonicity-induced increase in mucosal permeability and the osmolality-adjusting capability.

Experiments revealed that the stomach is resistant to hypotonic challenge while the jejunum is more sensitive to hypotonicity-induced increase in mucosal permeability than the duodenum. The hypotonicity-induced increase in duodenal mucosal permeability is not due to injury but possibly reflects physiological dilatation of paracellular shunts.

Luminal perfusion of the duodenum with an isotonic solution lacking Cl- decreased bicarbonate secretion while the lack of luminal Na+ increased mucosal permeability. Stimulation of bicarbonate secretion by COX-2 inhibition is to a large extent dependent on luminal Cl- while that induced by vasoactive intestinal peptide is not.

The hypotonicity-induced increase in mucosal permeability involves the release and action of serotonin (5-HT) on 5-HT3 and 5-HT4 receptors and stimulation of enteric nerves strongly implicating physiological regulation of this process.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2007. 59 p.
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 217
Physiology, luminal alkalinization, mucosal permeability, osmolality, cyclooxygenase-2, rat, duodenum, jejunum, motility, enteric nervous system, Fysiologi
urn:nbn:se:uu:diva-7444 (URN)978-91-554-6778-4 (ISBN)
Public defence
2007-02-02, B21, BMC, Norra vägen, Uppsala, 09:15
Available from: 2007-01-12 Created: 2007-01-12Bibliographically approved

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Sjöblom, Markus
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