F. B. Loud

Cysteamine-induced Duodenal Ulcer and Acid Secretion in the Rat

Duodenal ulcers can be produced in rats within 24 h by a single subcutaneous administration of cysteamine. To determine the role of gastric acid secretion in the pathogenesis of these ulcers, secretory and pathoanatomic studies were performed in chronic fistula rats ater an ulcerogenic dose of cysteamine. A prolonged increase of acid secretion was seen after cysteamine, reaching fourfold the basal level after 5 h. The acid response lasted for 10 to 11 h. After vagotomy cysteamine-induced acid secretion was markedly reduced. Ulcer formation was prevented by vagotomy and by drainage of the gastric juice before it entered the duodenum. When a gastric acid output equivalent to that produced by the ulcerogenic dose of cysteamine was induced by repeated injections of pentagastrin, no mucosal changes were seen in the duodenum. These results indicate that, although some acid in the duodenum is required for ulcer formation, the hypersecretion of acid induced by cysteamine is not the only factor responsible for the development of duodenal ulcer.

Zinc depletion in alcoholic liver diseases.

Liver and serum zinc concentrations were investigated in 24 patients with alcoholic liver diseases, 22 patients with non-alcoholic liver diseases, and in 36 control subjects. The liver samples were obtained by percutaneous liver biopsies, and the ratio of hepatocytes to fibrous connective tissue was estimated. The liver zinc concentration was expressed in relation to the amount of hepatocytes, and the serum zinc concentration was calculated in relation to total, albumin-, and alpha 2-macroglobulin-bound serum zinc. The results show that the liver zinc concentration was decreased in patients with alcoholic liver diseases (P < 0.01), in contrast to in patients with non-alcoholic liver diseases. Albumin-bound serum zinc was decreased in both groups (P < 0.001). The results indicate that alcoholic liver damage is associated with zinc deficiency.

Is somatostatin a humoral regulator of the endocrine pancreas and gastric acid secretion in man

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.

Colectomy for refractory constipation

Abstract Objective. This study evaluated the type of colectomy, postoperative complications, functional results, and satisfaction in patients with constipation refractory to conservative therapy. Further, colonic transit time (CTT), faecal load (coprostasis), and colon length (redundancies) were compared between operated and non-operated patients. Material and methods. Out of 281 patients, 30 women and 5 men underwent surgery. All patients were evaluated by clinical and physiological investigations. Forty-four randomly selected healthy persons constituted the control group. Results. Twenty-one patients had at hemicolectomy, 11 patients a subtotal colectomy and 3 patients an ileostomy. Two patients had an anastomotic leak and one died. In 11 patients, further surgery was necessary, because of recurrent constipation. Abdominal pain disappeared and defecation patterns improved significantly to 1–4 per day after a colectomy with no uncontrolled diarrhoea. The mean CTT was 65.0 h for patients operated, 37.9 h in non-operated patients and 24.75 h in controls (p < 0.05). Abdominal bloating and pain and defecation parameters correlated significantly positively with CTT and faecal loading, which were significantly increased in operated patients (p < 0.05). The colon was significantly longer in operated patients compared to non-operated, which significantly increased CTT and aggravated symptoms. The histology of the removed colon revealed degenerative changes. Conclusions. A segmental or a subtotal colectomy reduced bloating and pain and improved defecation patterns significantly. Although patient satisfaction was rather high, there are significant risks of postoperative complications and future operations. The operated patients had a significant increased CTT, faecal load and colon length, compared to non-operated patients.

Inhibition of meal-stimulated gastric acid secretion in man by exogenous and endogenous pancreatic glucagon.

The effect of intravenous infusion of glucagon (300 ng x kg(-1) x h(-1)), 1-arginine (0.6 g x kg(-1) x h(-1)) and of saline on meal-stimulated gastric acid secretion was studied in six healthy volunteers. Infusion of glucagon and 1-arginine enhanced plasma concentrations of pancreatic glucagon to 65--85 pmol/l, a level similar to that seen after a normal protein-rich meal. Both infusions significantly inhibited the acid response to the meal, most pronounced after 1-arginine. The difference in acid inhibition could not be ascribed either to differences in plasma glucagon concentrations or to differences in serum gastrin concentrations. The study supports the concept that pancreatic glucagon is a physiological inhibitor of gastric acid secretion.

Effect of endogenous pancreatic glucagon on gastric acid secretion in patients with duodenal ulcer before and after parietal cell vagotomy.

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.

Effect of arginine infusion on endogenous pancreatic glucagon and gastric acid secretion in duodenal ulcer patients and normal subjects.

The effect of intravenous infusion of L-arginine on pentagastrin-stimulated gastric acid secretion was studied in 15 duodenal ulcer patients and 12 healthy subjects. In both groups L-arginine enhanced plasma concentrations of pancreatic glucagon equally and to levels similar to those seen after a protein-rich meal and inhibited the acid response in duodenal ulcer patients and in normal subjects. The study supports previous findings suggesting that pancreatic glucagon is a physiological inhibitor of gastric acid secretion but does not support the hypothesis of a defect in this inhibitory system in duodenal ulcer patients.