Abstract
Abstract. Serum gastrin concentration and basal acid secretion were studied in normal subjects under the influence of respiratory acidosis induced by CO2 rebreathing. During the intragastric instillation of 100 ml/h 0·5 M bicarbonate a significant increase of gastrinaemia from 130 to 158 pg/ml (p < 0·01) occurred in ten subjects during respiratory acidosis (pCO2 62 torr, pH 7·25). Under the intragastric instillation of 100 ml/h 0·1 N HCl the rise of gastrin concentration in response to CO2 rebreathing (pCO2 68 torr, pH 7·20) was not significant. The relationship between the decrease of pH and the increase of the gastrin concentration was shifted in the direction of a greater systemic acidosis compared to the results performed in the presence of a neutral intragastric pH. 50 μg/kg propranolol intravenously produced a decrease of gastrin concentrations from 145 to 127 pg/ml (p < 0·01) and a total suppression of hyper‐gastrinaemia in response to CO2 rebreathing, suggesting activation of beta‐cell receptors in respiratory acidosis. The infusion of phentolamine in a dose of 0·6 to 1·8 mg/min. resulted in a rise of gastrin concentration from 140 to 165 pg/ml (p < 0·01) which was not further elevated during respiratory acidosis. The basal acid secretion showed a significant rise in response to CO2 rebreathing, which was abolished by the administration of propranolol.
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