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Background The effect of native somatostatin on Sphincter of Oddi motility still remains controversial. Sphincter of Oddi inhibition was demonstrated at manometry in patients in the acute phase of alcoholic pancreatitis. Other investigators showed marked somatostatin-induced impairment of bile flow by hepato-biliary scintigraphy. Aim Aim of the study was to determine the effects of therapeutical doses of exogenous somatostatin on Sphincter of Oddi motility. Patients and methods We studied eight patients (two men, six women, age 18–42), in the quiescent phase of idiopathic recurrent pancreatitis. We directly studied Sphincter of Oddi motility by perendoscopic manometry and, indirectly, secretin-stimulated pancreatic juice outflow by Ultrasound-Secretin test. The two tests were repeated before and after somatostatin infusion. Results Manometry was performed in two patients. After 250 μg somatostatin bolus the sphincter showed an increase of motor activity. At Ultrasound-Secretin test mean diameters were significantly larger at 40–60 min evaluation intervals during 250 μg/h somatostatin infusion as compared to saline infusion, showing a delayed pancreatic duct emptying. Conclusions Acute administration of somatostatin seems to induce an excitatory effect on Sphincter of Oddi motility, with impaired pancreatic outflow in patients in the quiescent phase of recurrent pancreatitis.

Summary The purpose of the present study is to evaluate the effect of carbenoxolone after a non-oral administration on the levels of prostaglandins E 2 and F 2α in gastric juice. The gastric secretion of 6 healthy volunteers (in basal conditions and after administration of a stimulus of 6 μg/kg weight of pentagastrin i.m.) was studied before and after seven days of treatment ment with 150 mg b.i.d. of carbenoxolone suppository. Concentration and output of prostaglandins E 2 and F 2α (measured by radioimmunoassay), hydrochloric acid, pepsin and N-acetyl-neuraminic acid in gastric juice were determined. Compared to control values, no statistically significant difference in acid, pepsin or prostaglandin F 2α content, or in gastric juice volume, was observed after treatment. However a significant increase was observed in the concentration and output of prostaglandin E 2 after administration of pentagastrin. The concentration and output of N-acetyl-neuraminic acid increased significantly only in basal conditions in carbenoxolone-treated subjects. The present study suggests that the cytoprotective action of carbenoxolone on gastric mucosa in man could be due to an increased prostaglandin E 2 activity. This effect is observed after rectal administration, therefore suggesting that carbenoxolone also has a systemic action.