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Department of Physiology, the Medical School, the University, Newcastle upon Tyne, NE1 7RU

1. The effect of I.V. administration of prostaglandin (PG) E₂ (10-40 µg kg^-1 h^-1), 16,16-dimethyl PGE₂ (0·1-0·5 µg kg^-1 h^-1), PGE₁ (16-20 µg kg^-1 h^-1), PGA₁ (5-11 µg kg^-1 h^-1) and PGF₂ (40 µg kg^-1 h^-1) on the relationship between [H⁺] and flow of gastric juice during stimulation of gastric secretion by pentagastrin was investigated in conscious cats prepared with cannulated gastric fistulae.

2. A- and E-type prostaglandins significantly reduced pentagastrin-stimulated acid output. This inhibition was associated with a reduction of the [H⁺] of the gastric juice such that the [H⁺] observed at any flow rate tended to be lower than the normal range observed with pentagastrin alone. With the highest doses of these prostaglandins the mean [H⁺] values were well below the normal range with pentagastrin alone.

3. At the dose tested, PGF₂ had little effect on acid output, and did not alter the relationship between [H⁺] and gastric flow.

4. There is a linear relationship between acid output and gastric flow and this relationship is similar during stimulation of gastric secretion by pentagastrin, histamine or insulin. Gastric acid inhibitory doses of cimetidine, atropine and somatostatin did not alter this relationship. In contrast the A- and E-type prostaglandins displaced this relationship to the right of the normal line observed with the acid stimulants alone. A- and E-type prostaglandins reduced the slope of the line relating acid output and gastric flow from 150-170 µequiv/ml^-1 to 100-120 µequiv ml^-1, this being taken as evidence of dilution of the parietal H⁺ secretion with a non-parietal secretion.

5. The volume of non-parietal gastric secretion was calculated as the gastric flow at zero acid output by extrapolation of linear plots of acid output versus gastric flow. Unstimulated gastric flow measured directly was 0·75 ml 15 min^-1. The calculated non-parietal flow was in the range 0·52-0·90 ml 15 min^-1 during stimulation of gastric secretion with pentagastrin, histamine and insulin, and inhibition of pentagastrin-stimulated acid secretion with cimetidine, atropine and somatostatin. PGE₂ (1·51 ml 15 min^-1) and 16,16-dimethyl PGE₂ (1·20 ml 15 min^-1) nearly doubled the calculated non-parietal flow.

6. These data demonstrate that gastric acid inhibitory doses of A- and E-type prostaglandins can reduce the [H⁺] in the bulk fluid of the gastric lumen during stimulation of acid secretion. The data provide evidence that these prostaglandins stimulate a non-parietal component of gastric secretion. This might be gastric bicarbonate and mucus secretion.