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Rat salivary gland ligation causes reversible secretory hypofunction

Authors :
Guy H. Carpenter
K. P. Paterson
Patricia Nunes Correia
S M Osailan
Gordon Proctor
Source :
Acta Physiologica (Oxford, England)
Publication Year :
2007
Publisher :
Wiley, 2007.

Abstract

Aim: To determine the influence of inflammation on salivary secretion. Secretion by salivary glands involves interactions between nerves, blood vessels and salivary cells. The present study investigated the effects of inflammation on rat submandibular gland function following acute ductal obstruction. Methods: Under recovery anaesthesia a metal clip was placed on the main duct of the submandibular gland. After 24 h salivary secretion was evoked by nerve and methacholine stimulation. For recovery experiments the clip was removed after 24 h and the animal left to recover for 3 days when salivary function was again assessed. Results: By 24 h of obstruction an inflammatory infiltrate had developed within the obstructed gland and stimulated salivary flows were just 20% of the normal secretion, whilst protein secretion and ion reabsorption were also severely impaired. If ductal obstruction was removed after 24 h the salivary function returned to normal after 3 days of recovery. In vitro analysis of cells from 24-h ligated glands revealed normal changes in intracellular calcium (the main secondary messenger involved in fluid secretion) in response to methacholine stimulation. Protein secretion from isolated cells indicated some changes in particular to methacholine-induced protein secretion although a significant protein secretion was still seen in response to isoprenaline – the main stimulus for protein secretion. Conclusion: This report demonstrates reversible salivary inhibition associated with an inflammatory infiltrate within the salivary gland.

Details

ISSN :
17481716 and 17481708
Volume :
189
Database :
OpenAIRE
Journal :
Acta Physiologica
Accession number :
edsair.doi.dedup.....90c7b537fa792ef973f144877ecad073
Full Text :
https://doi.org/10.1111/j.1365-201x.2006.01662.x