Effect of Atropine on Gastrin and Gastric Acid Response to Peptone Meal

Stanislaw J. Konturek; Jerzy Biernat; Jan Oleksy; Jens F. Rehfeld; Flemming Stadil

doi:10.1172/JCI107796

^{Institute of Physiology, Medical Academy, Kraków, Poland}

^{District Hospital, Karków, Poland}

^{Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, Denmark}

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^{Institute of Physiology, Medical Academy, Kraków, Poland}

^{District Hospital, Karków, Poland}

^{Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, Denmark}

Find articles by Biernat, J. in: JCI | PubMed | Google Scholar

^{Institute of Physiology, Medical Academy, Kraków, Poland}

^{District Hospital, Karków, Poland}

^{Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, Denmark}

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^{Institute of Physiology, Medical Academy, Kraków, Poland}

^{District Hospital, Karków, Poland}

^{Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, Denmark}

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^{Institute of Physiology, Medical Academy, Kraków, Poland}

^{District Hospital, Karków, Poland}

^{Department of Clinical Chemistry, Bispebjerg Hospital, Copenhagen, Denmark}

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Published in Volume 54, Issue 3 on September 1, 1974
J Clin Invest. 1974;54(3):593–597. https://doi.org/10.1172/JCI107796.
© 1974 The American Society for Clinical Investigation

Published September 1, 1974 - Version history

The action of intravenous atropine on meal-and pentagastrin-induced gastric acid secretion was studied in six duodenal ulcer patients.

A test meal of 10% peptone solution adjusted to pH 5.0 was maintained in the stomach at at distention presure of 15 cm H₂O, and a modification of the intragastric titration method of Fordtran and Walsh was used to measure gastric acid output by monitoring the rate at which a solution of 0.5 M sodium bicarbonate had to be added to keep the pH of the gastric content constant at the initial (pH 5.0) value. Serum gastrin concentrations were measured simultaneously by radioimmunoassy. The dose of 25 μg/kg-h atropine inhibited meal-induced acid secretion by about 70% and that evoked by pentagastrin by about 30%. The serum gastrin response to the test meal was not significantly altered by atropine.

We conclude that atropine is a very strong inhibitor of meal-induced gastric acid secretion and does not significantly change serum gastrin response to feeding in duodenal ulcer patients when postprandial gastric acidity (pH 5.0) and intragastric pressure (15 cm H₂O) are kept constant.

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