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Acta Physiologica 2012; Volume 206, Supplement 691
Scandinavian Physiological Society's Annual Meeting
8/24/2012-8/26/2012
Helsinki, Finland
MELATONIN REDUCES HYPOTONICITY-INDUCED INCREASES IN DUODENAL MUCOSAL PERMEABILITY IN RATS IN VIVO
Abstract number: P55
SOMMANSSON1 A, SJOBLOM1 M
1Department of Neuroscience, Division of Physiology, Uppsala University, Uppsala, Sweden
Introduction: Melatonin is released from enterochromaffin cells in the intestinal mucosa, but its influence on gastrointestinal function is still largely unknown. Our laboratory has recently showed that melatonin decreases duodenal mucosal paracellular permeability. In physiological situations the duodenal mucosa faces large variations of the luminal content. Ingestion of water creates a large gradient of tonicity between the lumen and the duodenal tissue that causes alterations in duodenal barrier function. It has previously been shown that hypotonic solutions increase duodenal paracellular permeability. The aim of the present study was to elucidate the effects of melatonin on hypotonicity-induced changes of duodenal barrier function.
Methods:
In anaesthetized rats a ~30 mm segment of the proximal duodenum with an intact blood supply was perfused in situ with saline, saline containing melatonin (50 mM), hypotonic NaCl solution (25 mM) or melatonin and hypotonic NaCl. Effects on duodenal mucosal permeability [blood-to-lumen clearance of 51Cr- EDTA], duodenal bicarbonate secretion (DBS), motility and net fluid flux were investigated.
Results:
The hypotonic NaCl solution (25 mM) did not alter DBS or motility but increased the paracellular permeability and decreased the net fluid flux. Luminal melatonin reduced the hypotonicity-induced increases in paracellular permeability but did not affect other parameters tested.
Conclusions:
Luminal perfusion of the duodenal segment with a hypotonic NaCl solution of 25 mM increases duodenal mucosal paracellular permeability. Administration of melatonin reduces the hypotonicity-induced increases in paracellular permeability.
To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 691 :P55