VAGAL NERVE AND THE GASTRIC-MUCOSAL DEFENSE

Citation
G. Mozsik et al., VAGAL NERVE AND THE GASTRIC-MUCOSAL DEFENSE, J PHYSL-PAR, 87(5), 1993, pp. 329-334
Citations number
24
Categorie Soggetti
Physiology
Journal title
JOURNAL OF PHYSIOLOGY-PARIS
ISSN journal
09284257 → ACNP
Volume
87
Issue
5
Year of publication
1993
Pages
329 - 334
Database
ISI
SICI code
0928-4257(1993)87:5<329:VNATGD>2.0.ZU;2-V
Abstract
An essential role for an intact vagal nerve has been proven in the dev elopment of gastric mucosal cyto- and general protection. On the other hand, chemically-induced (ethanol, HCI. indomethacin) gastric mucosal damage is enhanced after acute surgical vagotomy. The aims of this pa per were to study the possible mechanisms of the vagal nerve in the de velopment of gastric mucosal defense. The following questions were add ressed: 1) effect of surgical vagotomy on the development of ethanol- (ETOH), HCl-. and indomethacin (IND)-induced gastric mucosal damage. 2 ) changes in the gastric mucosal defense by scavengers, prostacyclin a nd other compounds (small doses of atropine and cimetidine: 3) changes in the gastric mucosal vascular permeability due to chemicals. 4) eff ect of indomethacin in the ETOH and HCl models with and without surgic al vagotomy: 5) changes in the gastric mucosal content of prostacyclin and PGE2 in the ETOH and HCl models after surgical vagotomy; and 6) c hanges in the role of SH-groups in gastric mucosal defense after surgi cal vagotomy. It was found that: 1) the gastric mucosal damage produce d by chemicals (ETOH. HCl. and indomethacin) was enhanced after surgic al vagotomy, 2) the cyto- and general gastric protective effects of be ta-carotene. prostacyclin, and small doses of atropine and cimetidine disappeared after surgical vagotomy: 3) the vascular permeability due to chemicals (ETOH. HCl. indomethacin) significantly increased after s urgical vagotomy in association with an increase in both number and se verity of gastric mucosal lesions; 4) IND alone (in animals with an in tact vagus) did not produce gastric mucosal lesions (in 1-h experiment s), but it aggravated ETOH-induced gastric mucosal damage (both its nu mber and severity): 5) the gastric mucosal levels of prostacyclin and PGE2 decreased after surgical vagotomy: 6) IND application (after surg ical vagotomy) decreased further the tissue levels of prostacyclin and PGE2 in association with an increase of gastric mucosal damage; and 7 ) the gastric mucosal protective effects of SH-groups were abolished b y surgical vagotomy.