Peptic Ulcer—A Review of the Literature for 1965

Kirsner, Joseph B.

doi:10.1016/s0016-5085(19)34399-9

Cited by 8 publications

(1 citation statement)

References 134 publications

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“…The concept of a gastric mucosal barrier, protecting the stomach against its own secretions, was developed by Code and by Davenport (Code, Higgins, Moll, Orvis & Scholer, 1963;Davenport, 1964;Davenport, Warner & Code, 1964) and, although the precise location and nature of this barrier has not been fully defined, its function may be performed in part by the mucus coating the surface of the stomach and in part by the apical plasma membrane of the surface epithelial cells (Avery Jones, 1975). It is now generally accepted that the integrity of the mucus cells of the stomach and their ability to secrete mucus continuously are essential protective mechanisms (Kirsner, 1966) but the precise role of mucus in the aetiology of gastric ulcers and erosions is unknown.…”

Section: Introductionmentioning

confidence: 99%

Effects of Fasting, Stress and Drugs on Gastric Glycoprotein Synthesis in the Rat

Dekanski

MacDonald

Sacra

et al. 1975

British J Pharmacology

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1The relationship between gastric mucosal damage and synthesis of gastric glycoproteins, as measured by the rate of incorporation of N-acetyl-[3 H]glucosamine, was investigated in rats after fasting and restraint stress and a single administration of aspirin (200 mg/kg, orally), phenylbutazone (200 mg/kg, orally), prednisolone (200 mg/kg, orally), or adrenaline (2 mg/kg, i.p.). In one experiment, the effects of aspirin and phenylbutazone on carbohydrate content of the glycoproteins were also determined. 2 Restraint stress, phenylbutazone and aspirin resulted in acute gastric mucosal erosions in some of the rats. Adrenaline produced severe sub-mucosal haemorrhage, but no erosions or ulceration, while prednisolone and fasting gave no gross pathology. 3 The rate of incorporation of N-acetyl-[3 H]glucosamine into glycoproteins was decreased after all treatments except adrenaline. In the groups receiving restraint stress, aspirin or phenylbutazone, the decreases were more marked in rats which developed erosions than in those with no gastric pathology. 4 Aspirin and phenylbutazone also produced changes in the carbohydrate content of the glycoproteins, the effects again being greater in the rats which developed erosions. 5 The results are discussed in the context of a possible association between erosion formation and glycoprotein synthesis and it is proposed that inhibition of mucus glycoprotein biosynthesis may be one mode of action of stress and drugs in causing gastric mucosal damage.

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