Effect of parenteral L-amino acids on gastric secretion and serum gastrin in normal dogs and dogs with portacaval transposition.

The effect of intravenous infusion of L-amino acids (FreAmine II) on gastric secretion and on circulating levels of gastrin was studied in five gastric fistula dogs and three dogs with portacaval transposition. Significant increases in gastric acid secretion were found after infusions which delivered 2.0, 4.0, and 8.0 gm/hr of L-amino acids in five gastric fistula dogs. After portacaval transposition, administration of amino acid solutions via the hindleg (through the liver) resulted in a great fall in the acid secretory response. Gastrin levels were significantly elevated after 8.0 gm/hr of amino acids. After 2.0 and 4.0 gm/hr, there was a slight but insignificant increase in serum gastrin levels. Gastrin levels were unchanged after infusion of 8.0 gm/hr of L-amino acids through the liver. We conclude that L-amino acids given intravenously stimulate gastric acid secretion in a dose-dependent manner by a mechanism which does not involve gastrin. At the highest dosage of amino acids, some gastrin was released which might have stimulated acid output further.

Effect of alcohol on the release of secretin and pancreatic secretion.

The effect of alcohol on the release of secretin was studied in man by radioimmunoassay, and in dogs and cats by radioimmunoassay and bioassay (secretion of water and bicarbonate by the pancreas). In man plasma secretin levels increased significantly from a basal of 121 +/- 14 to 164 +/- 24 pg/ml at 60 minutes after oral ingestion of alcohol. Intraduodenal administration of alcohol in man, dogs, and cats did not release secretin or affect pancreatic water and bicarbonate secretion in dogs and cats, but a moderate increase in pancreatic protein output was observed in these two species. Plasma gastrin levels rose significantly from a basal of 52 +/- 4 to 64 +/- 3 pg/ml after ingestion of alcohol in man and from 33 +/- 5 to 51 +/- 8 pg/ml after administration of alcohol into the stomach of dogs. Administration of alcohol into the duodenum in man, dogs, and cats did not release gastrin. We conclude that alcohol probably does not release secretin directly. The mechanism of release of secretin in man is unknown; it clearly involves the stomach and may be mediated via the release of gastric acid.

Influence of vagus on mechanisms for stimulation and inhibition of gastrin release.

In studies in dogs the gastrin response to food, to bombesin (1 micrgoram/kg-hr), and to somatostatin (2.5 and 5.0 microgram/kh-hr) plus food before and after truncal vagotomy was determined. Vagotomy caused an increase in basal levels of gastrin and in the release of gastrin after bombesin and food. Vagotomy augmented somatostatin suppression of food-stimulated gastrin release in a dose-dependent manner. We suggest that vagotomy causes a loss of both stimulatory and inhibitory vagal effects on gastrin release. Loss of vagal inhibition results in increased gastrin release to bombesin and food. Loss of vagal stimulation results in intensification of somatostatin-induced inhibition of postprandial gastrin release.

Intraoperative biochemical localization of insulinomas by quick radioimmunoassay.

In patients with organic hyperinsulinism, intraoperative determination of insulin concentrations in veins draining the pancreas might help localize the tumor. We have developed a radioimmunoassay measuring insulin within 30 minutes. At operation, blood samples are taken at various sites in the splenic, superior mesenteric and portal veins for insulin determinations. In all six patients, the highest insulin concentrations correlated with the site of the tumor. Also, small insulinomas less than 1 cm in diameter could be found. In one patient the tumor appeared to secrete mainly proinsulin. By this procedure we hope to avoid blind distal resection of the pancreas and possibly invasive preoperative diagnostic procedures.

Cholecystokinin is partly responsible for reduced food intake and body weight loss after total gastrectomy in rats.

PURPOSE: To determine the cause of body weight loss after total gastrectomy. METHODS: We evaluated the acute effect of exogenous cholecystokinin (CCK) on food intake and the chronic effect of CCK receptor blockade on food intake and body weight after total gastrectomy in rats. RESULTS: Exogenous CCK significantly reduced food intake in gastrectomized rats; this was blocked by administration of a CCK-A but not a CCK-B receptor antagonist. Chronic treatment with a CCK-A or CCK-B receptor antagonist after total gastrectomy in rats significantly increased postoperative food intake and body weight. CONCLUSION: Our data indicate that endogenous CCK is partly responsible for reduced food intake and body weight loss after total gastrectomy in rats.

[Disease picture and operative therapy in multiple endocrine adenomatoses (MEA sydrome)]. / Krankheitsbilder und operative Therapie bei multiplen endokrinen Adenomatosen (MEA-Syndrome).

We have outlined the symptoms, diagnostic procedures and operative treatment of "multiple endocrine adenomatosis" (MEA I, IIa und IIb). The priority of the operative procedure whenever two or more clinical syndromes in a patient with MEA are present and the possibility of multiple tumors has to be considered carefully. When there is a tumor of an endocrine organ, it should always bethought about the MEA-syndrome. We report about 9 patients seen in our hospital.

[10 years' results following proximal selective vagotomy in duodenal ulcer disease. A prospective study]. / 10-Jahres-Ergebnisse nach proximal selektiver Vagotomie beim Ulcus duodeni-Leiden. Eine prospektive Studie.

The results 10 years after proximal gastric vagotomy for chronic duodenal ulcer disease in a prospective trial are presented. Among 76 patients 5 were lost to follow-up, 3 had died from causes unrelated of ulcer disease. 80.3% of the patients remained clinically free from recurrence. 92.2% had a Visick grade I or II. The symptomatic recurrence rate was 19.7%, total recurrence rate including asymptomatic recurrences having been 25.3%. 6 patients (8.4%) had to be reoperated, 12 (16.9%) were treated medically. 3/4 of the medically treated patients only had 1 recurrence throughout 10 years. The rate of mild dumping and diarrhea was 2% each. Patients with recurrence showed no more significant reduction of BAO or pentagastrin stimulated maximal acid output (MAO) 10 years postoperatively. Patients without recurrence had a significant reduction of BAO and MAO of 42%. Based upon the results presented, the indication for proximal gastric vagotomy for chronic duodenal ulcer is still justified.

[Prevention and therapy of gastroduodenal stress bleeding with cimetidine]. / Prophylaxe und Therapie gastroduodenaler Stressblutungen mit Cimetidin.

In our intensive care unit we were able to prevent almost all bleedings from stress ulcerations in patients with insufficiency of various organs (1,6%) by administering the H2-receptor blocker cimetidine in doses of 8 X 200 mg per day. However, stress ulcer bleedings occurred in 14% of those patients also suffering from a sepsis. At lower doses of cimetidine, the rate of bleeding was comparable to that encountered in patients treated with antacids, i.e. 12,5% patients with multiple organ insufficiency and 42,7% with sepsis. Cimetidine was able to stop less extensive bleedings, but did not show any therapeutic effect in case of bleeding which led to a significant fall in hemoglobin concentration.

[Effect of hypophysectomy on gastrin release and antral gastrin concentration]. / Einfluss der Hypophysektomie auf die Freisetzung von Gastrin und die antrale Gastrinkonzentration.

Hypophysectomy resulted in a lower amount of basal serum gastrin. In hypophysectomized rats, there was a release of serum gastrin after food intake; however, the serum gastrin level was lower 30 min postprandially. The most important effect of hypophysectomy is absence of repletion of antral gastrin after an initial postcibarial depletion. We conclude that the immediate synthesis of antral gastrin after food intake is inhibited by hypophysectomy.

[Prevention and therapy of gastroduodenal stress hemorrhage in intensive care patients using the histamine H2-receptor antagonist cimetidine]. / Zur Prophylaxe und Therapie gastroduodenaler Stressblutungen bei Intensivpatienten mit dem Histamin-H2-Receptoren-Antagonisten Cimetidin.

In our intensive care unit we were able to prevent almost all bleedings from stress ulcerations in patients with insufficiency of various organs by administering the H2-receptor blocker, cimetidine, in doses of 200 mg eight times per day. However, stres ulcer bleedings occurred in 14% of those patients also suffering from a sepsis. At lower doses of cimetidine, the rate of bleeding was comparable to that encountered in patients treated with antacids, i.e. 12.5% patients with multiple organ insufficiency and 42.7% with sepsis. Cimetidine did not show any therapeutic effect in case of bleeding which led to a significant fall in hemoglobin concentration.

[Postoperative recurrent gastroduodenal ulcer: pathogenesis--reinterventions--results]. / Das postoperative gastroduodenale Rezidivulcus: Pathogenese--Reinterventionen--Ergebnisse.

High 10-year recurrence rates following proximal gastric vagotomy (PGV) for pyloric/prepyloric ulcer (31.6%, European trial) result from antral stasis (Dragstedt-mechanism). Additional pyloroplasty reduces the recurrence rate to 16.6%. General causes of recurrence following PGV are primarily incomplete vagotomy and smoking: For incomplete vagotomy (Burge-test) 24.4% recurrences, for complete vagotomy 13.6% (10-year results); in smokers 38%, non-smokers 12%. Therapy is conservative in 80%. Selective gastric revagotomy and antrectomy as reoperation shows lowest recurrence rate (1.2%). The major cause of recurrence after partial gastrectomy is inadequate resection. Conservative therapy is successful in 76%. Reoperation should be transthoracic vagotomy with no mortality in 11 centers.

Surgical intervention following fragmentation of gallstones by extracorporeal shock waves.

Five cases of surgical intervention following extracorporeal shock wave lithotripsy (ESWL) of gallbladder and bile duct stones are reported. This represents an incidence of surgical intervention in 1% of patients with gallbladder stones and in 9% of patients with common bile duct stones who underwent ESWL during a two-and-a-half-year investigation period. There was no mortality. In 2 patients with gallbladder stones and persistent colic after ESWL, elective cholecystectomy was performed. There was no evidence of macroscopic or microscopic damage or bleeding within the wall of the gallbladder. Furthermore, no damage to the liver, common bile duct, duodenum, or stomach was noted. ESWL was applied in 34 patients with common bile duct stones in whom endoscopic sphincterotomy and stone extraction had proved ineffective. Three (9%) of these patients required surgery. In 1 patient, a Dormia basket got stuck and the basket, together with the stone, were removed by choledochotomy. In a second patient, rupture of a juxtapapillary diverticulum occurred 10 days after ESWL and 2 days after endoscopic extraction of stone fragments. At laparotomy, the retroperitoneum was drained. In a third patient with gallbladder and common bile duct stones, acute cholecystitis developed after lithotripsy of common bile duct stones. Cholecystectomy was performed and a t-tube was inserted in the bile duct. In all patients, the postoperative course was uneventful. In our experience, ESWL is a safe procedure with no mortality and an infrequent need for surgical intervention.

Physiologic release of secretin measured in peripheral and portal venous blood of dogs.

The effect of food on circulating levels of secretin, measured by radioimmunoassay, was studied in 7 dogs. Significant postprandial increases in secretin were found in portal and peripheral plasma of dogs fasted for 18 h. Basal levels of secretin were significantly lower in dogs fasted for 72 h when compared with dogs after an 18-hour fast. After the prolonged fast, food caused a significant release of secretin, measured peripherally. We conclude that secretin is released by a physiologic stimulus (food) and that circulating levels of secretin are depressed after prolonged starvation.