Role of vagal nerve in defence mechanisms against nsaid-induced gastrointestinal mucosal damage

G. Mózsik, O. M E Abdel-Salam, B. Bódis, O. Karádi, L. Nagy, J. Szolcsányi

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Results: (1) acute surgical vagotomy aggravated, whereas, chemical vagotomy prevented the GI mucosal damage produced by topically and systemically applied NSAIDs; (2) indomethacin produced significantly more damage in the small intestine than in the large bowel and stomach (order is small intestine > stomach > proximal colon) which is aggravated by acute surgical vagotomy in all these areas of the GI tract; (3) stimulation of capsaicin-sensitive sensory nerves with the capsaicin analogue resiniferatoxin protected against gastric mucosal damage by acidified salicylates and indomethacin; (4) chemical deafferentation enhanced the aspirin-induced gastric mucosal injury, while it did not interfere with the prostacyclin-induced gastric cytoprotection; (5) the mucosal protective effects of PGI2, atropine, cimetidine, sucralfate and scavengers (β-carotene) disappeared after acute surgical vagotomy. Many papers suggested only an aggressive role of the vagus nerve on the gastrointestinal (GI) mucosa; however, the essential role of the vagus nerve was proven in GI mucosal defence against different chemicals, e.g., ethanol, HCl, non-steroidal anti-inflammatory drugs (NSAIDs). In order to evaluate the role of the vagus nerve in the development of GI mucosal damage evoked in the rat by the administration of NSAIDs, the present studies were designed to: (1) compare the changes in the NSAID-induced GI mucosal damage after acute surgical and chemical (atropine treatment) vagotomy; (2) investigate the effect of sensory nerve stimulation and chemical deafferentation on the NSAID-induced gastric mucosal damage; (3) evaluate the cytoprotective action of prostacyclin under the above experimental conditions; (4) study the effect of surgical vagotomy on the gastroprotection induced by different drugs. Gastric mucosal damage was produced by intragastrically (acidified salicylates) or systemically (indomethacin) applied NSAIDs, while the small intestinal and large bowel mucosal injury was produced by systemic indomethacin application.

Original languageEnglish
Pages (from-to)151-172
Number of pages22
JournalInflammopharmacology
Volume4
Issue number2
DOIs
Publication statusPublished - Jun 1996

Fingerprint

Vagotomy
Stomach
Anti-Inflammatory Agents
Indomethacin
Vagus Nerve
Epoprostenol
Gastrointestinal Agents
Pharmaceutical Preparations
Salicylates
Capsaicin
Atropine
Small Intestine
Sucralfate
Chemical Stimulation
Cytoprotection
Cimetidine
Wounds and Injuries
Carotenoids
Aspirin
Gastrointestinal Tract

Keywords

  • atropine
  • capsaicin-sensitive sensory nerves
  • gastric acid secretion
  • GI mucosa
  • H back-diffusion
  • mucosal biochemistry
  • mucosal PG and PGI
  • NSAIDs
  • surgical vagotomy

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)
  • Immunology

Cite this

Role of vagal nerve in defence mechanisms against nsaid-induced gastrointestinal mucosal damage. / Mózsik, G.; Abdel-Salam, O. M E; Bódis, B.; Karádi, O.; Nagy, L.; Szolcsányi, J.

In: Inflammopharmacology, Vol. 4, No. 2, 06.1996, p. 151-172.

Research output: Contribution to journalArticle

Mózsik, G. ; Abdel-Salam, O. M E ; Bódis, B. ; Karádi, O. ; Nagy, L. ; Szolcsányi, J. / Role of vagal nerve in defence mechanisms against nsaid-induced gastrointestinal mucosal damage. In: Inflammopharmacology. 1996 ; Vol. 4, No. 2. pp. 151-172.
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