Microscopic Analysis of Ethanol Damage to Rat Gastric Mucosa After Treatment With a Prostaglandin

Lacy, Eric R.; Ito, Susumu

doi:10.1016/s0016-5085(82)80198-4

Cited by 348 publications

(55 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Histological examination indicated that DSCG protected the mucosa against damage, although in one animal out of four, the drug was unable to prevent slight desquamation of the superficial epithelial cell layer. As such, cytoprotection by DSCG resulted in a histological pattern almost identical to that found for protanoids (Lacy & Ito, 1982;Schmidt el al., 1985). In spite of this similarity, however, it proved difficult to obtain clear evidence for a role ofendogenous prostaglandins in the process of cytoprotection by DSCG.…”

Section: Discussionmentioning

confidence: 55%

Cytoprotective effects of disodium cromoglycate on rat stomach mucosa

Goossens

Reempts

Wauwe

1987

British J Pharmacology

View full text Add to dashboard Cite

The cytoprotective effects of the anti‐asthmatic drug, disodium cromoglycate (DSCG), on gastric mucosal necrosis induced by ethanol in rats were studied. Subcutaneous, but not oral, DSCG prevented the formation of gastric lesions and this effect was dose‐dependent between 1.25 and 40 mg kg−1, with an ED50 value of 6.8 mg kg−1. Maximal cytoprotection occurred 15–30 min after DSCG treatment. Histological examination revealed that DSCG effectively protected the gastric mucosa against ethanol‐induced vascular congestion, haemorrhage, epithelial desquamation and mucosal oedema. Enhanced production of endogenous prostaglandins, which are known cytoprotective compounds, could not explain the mucosal protection. At a dose of 40 mg kg−1, DSCG did not change prostaglandin E2 or 6‐keto‐prostaglandin F1α concentrations in gastric mucosal tissue, although its cytoprotective activity was partially inhibited by prior treatment of the animals with indomethacin.

show abstract

Section: Discussionmentioning

confidence: 55%

Cytoprotective effects of disodium cromoglycate on rat stomach mucosa

Goossens

Reempts

Wauwe

1987

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…It is well known that ethanol produces gastric mucosal damage within 1-3 min of its instillation into the gut and lasts for more than 2 h by causing areas of focal hyperaemia and haemorrhage. 23 Moreover, intragastric ethanol increases vascular permeability and vascular damage 24 occurring in capillaries near the luminal surface and not in the deeper muscularis mucosa, which indicates a role for impaired blood flow in the genesis of AE-induced gastric lesions.…”

Section: Discussionmentioning

confidence: 99%

A Comparative Study On The Activity Of Lansoprazole, Omeprazole And PD‐136450 On Acidified Ethanol‐ And Indomethacin‐Induced Gastric Lesions In The Rat

Chandranath

Bastaki

Singh

2002

Clin Exp Pharma Physio

View full text Add to dashboard Cite

1. The proton pump inhibitors lansoprazole (LP) and omeprazole (OP) and the cholecystokinin (CCK)-receptor antagonist PD-136450 (PD) provide a broad spectrum of activities in their ability to inhibit gastric acid secretion and protect the stomach against ulcerogens. In the present study, we investigated the protective effects of these compounds against gastric ulcers induced by acidified ethanol (AE) and indomethacin. 2. Both AE (60% ethanol in 150 mmol/L HCl, 1 mL/rat) and indomethacin (30 mg/kg) produced gastric haemorrhagic lesions in the rat 1 and 6 h after oral administration, respectively. 3. The gastric mucosal protective effects of LP (1-20 mg/kg), OP (0.5-10 mg/kg) and PD (1-20 mg/kg), administered either orally or subcutaneously (s.c.) 30 min before the administration of AE or indomethacin, were dose dependent against both models of ulcer induction. 4. To determine whether the cytoprotective effect of LP, OP and PD (each 10 mg/kg) was mediated by endogenous prostaglandins (PG), indomethacin (10 mg/kg, s.c.) was administered 15 min before AE to inhibit prostanoids biosynthesis. Indomethacin reduced the cytoprotective effects of OP, but not LP, administered either orally or s.c. Indomethacin reduced the cytoprotective effect of PD administered orally, although the effect was much less significant than when PD was administered s.c. The results exclude the role of PG in mediating the protective effects of LP, whereas the possibility exists for PG to have a role in mediating the protective effects of OP and PD. 5. To investigate the possible involvement of endogenous nitric oxide (NO) in the cytoprotective action of LP, OP and PD, we treated rats with a selective inhibitor of NO synthesis, namely NG-nitro-L-arginine methyl ester (L-NAME; 25 mg/kg, s.c.). Administration of L-NAME 15 min prior to LP, OP or PD (each 10 mg/kg) orally or s.c. and challenge with AE or indomethacin did not significantly increase the degree of the ulcer index and L-NAME was not able to antagonize the protective effects of LP, OP and PD, thus excluding the role of NO in mediating the protective effects of these drugs. However, the effects of PD in reducing the indomethacin-induced ulcer index were less significant in the presence than the absence of L-NAME (P < 0.05 vs P < 0.001, respectively), suggesting a role for NO. 6. In conclusion, the results of the present study suggest that LP and OP are equally effective against AE- as well as indomethacin-induced gastric ulcers and were more potent than PD in protecting the stomach against ulcer formation. Lansoprazole, OP and PD bring about their cytoprotective action through the reduction of acid secretion and some other unknown mechanisms. However, OP and PD may exert their cytoprotective action through PG and NO pathways.

show abstract

“…Gastric mucosal damage by various agents, including ethanol, has been shown to be prevented by pretreatment with PGI, (Mozsik rt a/., 1982). The cytoprotective action of PGI, may result from its ability to prevent deep mucosal vasocongestion and associated necrotic lesions of the glandular tissue (Lacy and Ito, 1982). Since the discovery and structural elucidation of PGI,, several studies have revealed its inhibitory influence on platelet aggregation, but in citro and in vivo (McGiff, 1981).…”

Section: Resultsmentioning

confidence: 99%