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  • Title: Determination of acid-neutralizing capacity in rat duodenum. Influences of 16,16-dimethyl prostaglandin E2 and nonsteroidal antiinflammatory drugs.
    Author: Takeuchi K, Furukawa O, Tanaka H, Okabe S.
    Journal: Dig Dis Sci; 1986 Jun; 31(6):631-7. PubMed ID: 3709328.
    Abstract:
    A model involving measurement of duodenal pH and acid-neutralizing capacity has been devised in anesthetized rats. A duodenal loop was made between the pyloric ring and the area just proximal to the outlet of the common bile duct (2 cm) and was perfused at a flow rate of 1.3 ml/min with HCl solution (1 X 10(-4) M, pH 4.0) made isotonic with NaCl. The pH of duodenal perfusate was continuously measured using a pH glass electrode of the flow type, and the amount of acid neutralized in the loop was titrated to pH 4.0 using a pH-stat method and by adding 10 mM HCl. Under normal conditions, the duodenal pH was kept around 6.0 as the result of neutralization in the loop (approximately 9 mu eq/hr). Subcutaneous administration of 16,16-dmPGE2 (10 micrograms/kg) significantly elevated the pH and increased acid-neutralizing capacity to 168.3% of normal levels. In contrast, indomethacin (5 mg/kg) and aspirin (200 mg/kg) as cyclooxygenase inhibitors or quinacrine (100 mg/kg) as a phospholipase A2 inhibitor significantly decreased both the pH and acid neutralizing capacity. After sacrifice with saturated KCl (intravenously), the pH decreased to 4.3 +/- 0.2 and the neutralizing capacity was reduced to 30% of normal values. Basal HCO3- secretion in the proximal duodenum (approximately 5 mu eq/hr), when titrated to pH 7.4, was significantly stimulated by 16,16-dmPGE2 and exposure of the mucosa for 10 min to 10 mM HCl. Neither indomethacin, aspirin, nor quinacrine had any effect on basal HCO3- secretion, but all significantly inhibited HCl-stimulated HCO3- secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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