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Titolo:
NICOTINE AND GASTRIC-ULCERS IN STRESS
Autore:
OGLE CW; QIU BS; CHO CH;
Indirizzi:
UNIV HONG KONG,FAC MED,DEPT PHARMACOL,5 SASSOON RD HONG KONG HONG KONG
Titolo Testata:
JOURNAL OF PHYSIOLOGY-PARIS
fascicolo: 6, volume: 87, anno: 1993,
pagine: 359 - 365
SICI:
0928-4257(1993)87:6<359:NAGIS>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
COLD-RESTRAINT STRESS; ZINC-SULFATE; RATS; ULCERATION; ETHANOL; STIMULATION; STOMACH; INJURY;
Keywords:
GASTRIC ULCERS; STRESS; CHOLINERGIC RECEPTORS; NICOTINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
32
Recensione:
Indirizzi per estratti:
Citazione:
C.W. Ogle et al., "NICOTINE AND GASTRIC-ULCERS IN STRESS", J PHYSL-PAR, 87(6), 1993, pp. 359-365

Abstract

Chronic nicotine treatment worsens stomach mucosal damage by cold (4-degrees-C) and restraint (stress) : it dose- and time-dependently intensifies stress-evoked gastric glandular ulceration, mast cell degranulation and motility. Nicotine 50 mug/ml drinking water, given ad libitum to female Sprague-Dawley rats for 10 days. increases the sensitivityof the isolated stomach strip to acetylcholine-induced contractions: atropine abolishes this action. The isolated anococcygeus muscle from nicotine-treated male rats shows increased sensitivity to noradrenaline-induced contractions, but not to those by acetylcholine. Hexamethonium or atropine pretreatment antagonises stress-induced gastric effectsin nicotine-drinking rats. Muscarinic M1- and M2-, but not M3-. receptor block (by pirenzepine. AF-DX 116BS and HHSiD, respectively) inhibits stress ulcer formation in female rats. Although tobacco smoking hasbeen reported to increase free radical formation. mucosal xanthine oxidase which initiates free radical formation is uninfluenced by nicotine: antagonising this enzyme (by allopurinol) or hydroxyl free radicalscavenging (by dimethylsulfoxid) does not lessen the effect of nicotine on stress-evoked ulceration. The findings suggest that chronic nicotine treatment produces partial ganglionic blockade of the vagal nervewhich leads to muscarinic receptor supersensitivity. This phenomenon contributes significantly to the ulcer-worsening mechanism: muscarinicM1- and M2-receptors appear to be involved. The gastric ulcer-aggravating effect of nicotine in stressed rats appears not to be due to increased free radical formation.

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Documento generato il 01/10/20 alle ore 06:06:21