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P E O'Brien

Publications and source records attributed to P E O'Brien.

76 records · Page 5Linked to original sources
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Time as a factor in the expression of ethanol injury to the gastric mucosa.

A technique of quantitative histology was used to assess the influence of time after injury on the histological expression of gastric mucosal damage. Rats, pretreated with either natural prostaglandin E2 or saline, were subjected to intragastric administration of either 50% or 100% ethanol. Fifteen minutes later the ethanol was removed from the stomach. Rats were sacrificed at either 30 min or 24 h after ethanol instillation. In rats pretreated with saline and subjected to 100% ethanol with or without prostaglandin pretreatment, the extent of deep mucosal damage was markedly underestimated by early evaluation. Only 5.4% of the volume of the gastric mucosa showed evidence of damage at 30 min after ethanol, compared with 57.3% of the volume of the mucosa, at 24 h after 100% ethanol exposure. Assessment of gastric mucosa 24 h after ethanol injury showed that PGE2 reduces the extent of surface area damaged and the volume of the mucosal damage. When 50% ethanol was used as the injurious agent, no difference was noted in the volume of the mucosa damaged when the stomach was assessed at either 30 min or 24 h after injury. These results indicate that full histological expression of injury is not present 30 min after 100% ethanol instillation, at least in part because of fixation of the gastric mucosa by 100% ethanol. Fifty per cent ethanol, which does not cause mucosal fixation, may be better as a test agent.

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PubMedDate not supplied

The role of luminal factors in prostaglandin protection against ethanol-induced gastric mucosal injury.

Prostaglandins (PG) protect the gastric mucosa against damage by several irritants, but the mechanisms remain unclear. A standard rat model of gastric injury induced by 50% ethanol was used to test the hypothesis that PG protection occurs either by increasing luminal fluid volume and hence diluting the irritant, or by production of protective factors within this fluid. Quantitative histology was used to assess microscopic mucosal damage. The increase in luminal fluid volume in prostaglandin E2 (PGE2)-treated animals was measured, and the ability of this increased fluid to protect saline-treated animals via dilution of the irritant was assessed. The transfer of protection by exchange of luminal fluid from PG to non-PG treated animals was also tested. Results showed that PGE2 induced a specific increase in luminal fluid volume of 45.6%. When given together with ethanol treatment the extra fluid volume was not protective. Removal of luminal fluid after PG and before ethanol treatment did not abolish protection and no protective factor was transferred with the luminal fluid. In conclusion, this study has shown that neither dilution of ethanol by accumulation of luminal fluid nor the presence of luminal factors is responsible for PG protection.

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PubMedDate not supplied

Sulphated macromolecules produced by in vivo labelling in the rat gastric mucosa.

The aim of this study was to investigate the nature and distribution of sulphated macromolecules of the extracellular matrix in rat gastric mucosa. This was achieved by developing an in vivo labelling system. An intraperitoneal injection of 1 mCi [35S]-sulphate was given for either 4 h (0.01% incorporation into macromolecular fraction) or 8 h (0.13% incorporation). At the end of the labelling period the stomach was removed and the mucosa and submucosa was either taken as a single combined sample or separated into four layers by blunt dissection. Each sample was papain digested and analysed by ion-exchange chromatography. This analysis revealed sulphated species of differing charge existing in differing proportions throughout the mucosa. These sulphated species eluted at NaCl concentrations of approximately 0 (A), 0.19 (B), 0.34 (C) and 0.78 mol/L (D) from a Q-Sepharose ion exchange column. Further analysis by size exclusion chromatography and chemical and enzymatic digestion showed that peaks B and C had molecular weights of 2.4 x 10(5) and 2.8 x 10(5), respectively and were resistant to chondroitinase ABC, heparitinase and nitrous acid digestion. Peak D was found to contain a polydisperse population of molecules with a molecular weight range of approximately 1 x 10(4) to 6 x 10(4). This sample was susceptible to nitrous acid and chondroitinase ABC digestion and was found predominantly in the sample isolated from deeper in the tissue. We have thus developed an in vivo labelling technique for sulphated macromolecules that can be used in the further study of injury to the gastric mucosa.

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