Partial sleep deprivation compromises gastric mucosal integrity in rats

Partial sleep deprivation compromises gastric mucosal integrity in rats

Copyright © 2005 Elsevier Inc. All rights reserved.


Jin Sheng Guoa, b, Jenny Fung Ling Chaua, Chi Hin Choa and Marcel Wing Leung Kooa, ,

aDepartment of Pharmacology, Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong, China

bDivision of Digestive Diseases, Department of Internal Medicine, Zhong Shan Hospital, Fu Dan University, Shanghai, 200032, China

Received 27 June 2004; accepted 29 December 2004. Available online 3 February 2005.

Abstract

The gastric mucosa is most susceptible to stress that has been shown to induce mucosal damage in humans and animals.

This study aims to explore the underlying mechanisms of partial sleep deprivation, as a source of psychophysiological stress, on gastric functions and its effect on mucosal integrity.

Sprague-Dawley rats were partially sleep deprived (PSD) for 7 or 14 days by housing inside slowly rotating drums.

Gastric tissues and plasma were sampled at the end of the sleep deprivation periods and mucosal lesion scores were evaluated.

Morphological examination was performed after Hematoxylin and Eosin staining.

Plasma levels of noradrenaline, adrenaline, gastrin, histamine and somatostatin were determined with enzyme immunoassays.

Gastric acidity was measured with acid-base titration in pylorus ligated rats.

Gastric mucosal blood flow was evaluated with Laser Doppler Flowmetry.

It was found that gastric lesions were induced in about 30%–50% of the PSD rats.

Gastric acidity as well as plasma levels of noradrenaline, gastrin and histamine were elevated.

Gastric mucosal blood flow and plasma somatostatin level were on the contrary reduced, especially in rats with PSD for 14 days.

It is concluded that partial sleep deprivation compromises gastric mucosal integrity by increasing gastric acidity, plasma levels of noradrenaline, gastrin, histamine, and decreasing gastric mucosal blood flow.

These results provided experimental evidence on the gastric damaging effects of PSD and it could be one of the risk factors contributing to gastric ulcer formation.

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