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A dose response study of the effect of an octapeptide somatostatin analogue, SMS 201-995, on meal stimulated gastric acid secretion was carried out in 12 healthy volunteers. Infusion of SMS 201-995 in a dose of 50 pmol/kg/h almost completely abolished the acid response to the meal. Pl-gastrin was significantly decreased during infusion of 10 pmol/kg/h of SMS 201-995 and insulin was significantly inhibited during infusion of 50 pmol/kg/h. SMS 201-995 in a dose of 50 pmol/kg/h inhibited basal and submaximal pentagastrin stimulated acid secretion by 77% and 84% respectively (p less than 0.01). On a molar basis SMS 201-995 is substantially more potent than natural somatostatin in inhibiting gastric acid secretion. [ABSTRACT FROM PUBLISHER]

The effect of low dose infusions of somatostatin on meal stimulated gastric acid secretion was studied in eight healthy volunteers by intragastric titration after a peptone test meal with radioimmunoassay control of the plasma concentrations of somatostatin and the pancreatic hormones glucagon and insulin. Infusion of somatostatin in a dose of 100 ng/kg/h, resulting in a plasma concentration of 13.4 +/- 2.1 pmol/l, inhibited acid secretion significantly, and in a dose of 800 ng/kg/h, with corresponding plasma concentration of 66.5 +/- 12.0 pmol/l the acid secretion was virtually abolished. Plasma concentrations of insulin and pancreatic glucagon decreased significantly during infusion of 200 ng/kg/h (24.5 +/- 7.5 pmol/l) and glucose concentrations increased. Serum gastrin was only significantly decreased during the highest dose of somatostatin. The range of plasma somatostatin concentrations obtained with the lower doses correspond to reported physiological variations. The results support the concept that somatostatin participates in the hormonal control of the pancreatic endocrine and the acid secretion. [ABSTRACT FROM PUBLISHER]

The effect of endogenous pancreatic glucagon on submaximal pentagastrin stimulated gastric acid secretion was studied by infusion of 1-arginine in patients with duodenal ulcer before and after parietal cell vagotomy without drainage (PCV). Preoperatively infusion of 1-arginine resulted in a marked inhibition of acid secretion, whereas no effect was found postoperatively. Plasma glucagon concentrations were identical pre- and postoperatively, fasting as well as during arginine infusion. Serum gastrin concentration rose after PCV but not unaffected by arginine infusion both pre- and postoperatively. The study demonstrates that intact vagal innervation of the fundic glands is a condition of inhibition of pentagastrin induced acid secretion by pancreatic glucagon released by infusion of 1-arginine. [ABSTRACT FROM PUBLISHER]

Cysteamine in a single subcutaneous administration induces release of gastrin, acid hypersecretion, and duodenal ulcer in rats. Pentagastrin-induced acid hypersecretion has no ulcerogenic effect. The Brunner glands in the proximal duodenum have previously been shown to be an important factor in the natural defence of the duodenal mucosa, and this study has been performed to determine the effect of cysteamine and pentagastrin on the Brunner glands in the rat. The proximal duodenum was isolated in situ and drained by a polyethylene tube. The secretion was studied for two 5-h periods after administration of cysteamine or pentagastrin, and then the Brunner glands were studied histologically. Pentagastrin did not affect spontaneous Brunner gland secretion, whereas cysteamine inhibited the output approximately 50%. After cysteamine the secretory cells were low and depleted of mucus, suggesting that cysteamine interferes with the synthesis of the secretory product. The depression of the Brunner gland secretion may be an important factor in the pathogenesis of cysteamine-induced duodenal ulceration.

A prospective, randomized, controlled trial was conducted to compare truncal vagotomy and drainage (TV), selective vagotomy and drainage (SV) and parietal cell vagotomy (PCV) as elective treatment for duodenal ulcer. Between 11 and 15 years post-operatively, 248 patients were available for study of the recurrent ulceration rate by a life table method and 197 patients could be studied with regard to post-vagotomy symptoms. The recurrent ulcer rates were TV 28.5%, SV 37.4% and PCV 39.3%. These differences were not statistically significant. There was no significant difference in the Visick gradings among the three groups either before or after treatment of the failures. About two-thirds of the patients in each group were finally satisfied with their operation, often after second operations or prolonged medical treatment.

A prospective, randomized, controlled trial was conducted to compare truncal vagotomy and drainage (TV), selective vagotomy and drainage (SV) and parietal cell vagotomy (PCV) as elective treatment for duodenal ulcer. Between 11 and 15 years after operation, 248 patients were available for study of the recurrent ulceration rate by a life table method, and 197 patients could be studied with regard to postvagotomy symptoms. The recurrent ulcer rates were 28.5% for TV, 37.4% for SV, and 39.3% for PCV. These differences were not statistically significant. The incidence of severe postvagotomy symptoms was as follows: dyspepsia, 18.4% for TV, 20.5% for SV, 8.6% for PCV; dumping, 5.9% for TV, 19.6% for SV, 2.2% for PCV; diarrhea, 9.8% for TV, 11.8% for SV, 4.4% for PCV. The incidence of severe dumping was significantly less frequent among the PCV patients than the SV group. The differences did not reach statistical significance in any of the other groups. There was no significant difference in the Visick gradings among the three groups either before or after treatment of the failures. About two thirds of the patients in each group were finally satisfied with their operation, often after second operations or prolonged medical treatment. It is concluded that none of the three forms of vagotomy can be recommended as the standard operative treatment of duodenal ulceration.