In order to investigate the effect of pancreatic glucagon on gastric secretion, serum gastrin levels and the fluid output, acid output of gastric juice were measured after intravenous injection of glucagon (1mg/1ml) in five Heidenhain pouch dogs under the oral administration of glycine solution. Glycine-induced hypergastrinemia was inhibited by intravenous injection of glucagon, and also fluid output and acid output were inhibited. However, this inhibition of gastric secretion was not significantly related to changes of serum calcium levels and blood sugar levels. These results suggested that the inhibition of gastric secretion by glucagon was mainly due to the inhibition of release of endogenous gastrin.

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The present study was performed to investigate gastric secretion and serum gastrin levelsafter ligation of the pancreatic duct in Heidenhain pouch dogs.
The results obtained were summarized as follows:
Serum gastrin levels began to elevate from the second week and reached high levels at the fourth week after a complete pancreatic duct ligation. However, the elevation of serum gastrin levels was not markedly after a simple pancreatic duct ligation. Gastric hypersecretion and hypergastrinemia were confirmed by the oral administration of glycine solution in dogs after a complete pancreatic duct ligation. Ulcer was observed in the stomach or Heidenhain pouch by pathological examination. Glycine-induced gastric hypersecretion and hypergastrinemia could be inhibited by intravenous injection of glucagon.
These results suggested that the origin of oversecreted gastrin after a complete pancreatic duct ligation was mainly from the gastric antrum.

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The effects of various types of vagotomy such as TV, SV, SPV and selective antral vagotomy on gastrin release and gastric secretion were studied. In acute experiments, 8 dogs received insertions of warm water into their stomachs to obtain gastric distension, and the subsequent change in serum gastrin concentration was determined by radioimmunoassay. In chronic experiments, the Heidenhain pouch was prepared in 13 dogs, and serum gastrin concentration and Heidenhain pouch secretion were determined under stimulated or nonstimulated conditions before and after various types of vagotomy. The former concentration was determined by the above-mentioned method.
Results are as follows:
1) In the acute experiments, a moderate increase in serum gastrin concentration was demonstrated in the dogs which received SPV, while a decrease occurred in the dogs which received other types of vagotomy.
2) The following results were obtained from the chronic experiments.
i) Gastric secretion from the histamine-stimulated pouches was reduced after every type of vagotomy.
ii) Gastric secretion from the meal-stimulated pouch was increased, and serum gastrin level was also increased in such dogs after every type of vagotomy.
iii) Serum gastrin level following insulin-induced hypoglycemia was increased after SPV, TV and SV and reduced after selective antral vagotomy.
iv) Gastric secretion from the pouch in the dogs treated with insulin was increased after SPV and reduced after other types of vagotomy.
These results led to the conclusion that there was no corelation between the level of serum gastrin and the acid output from the Heidenhain pouch following feeding or treatment with insulin before and after various types of vagotomy.

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The inhibition of pancreatic exocrine secretion by hypertonic glucose and amino acids infusion was studied in dogs with chronic pancreatic fistula and open gastric fistula. Under the background infusion of secretin and pancreozymin, 20% glucose, 30% glucose and 12% amino acids were given by intravenous infusion for an hour. Bicarbonate concentration were not showed an inhibitory, but showed depression in volume and enzyme secretion. Maximal percent decrease in volume and amylase output by infusion of each solutions were 23% and 11% (20% glucose), 32% and 29% (30% glucose) and 53% and 42% (12% amino acids) respectively. In infusion of hypertonic glucose, it was appeared parallel in the effect of inhibitory with degree of elevation in blood sugar and IRI. IRI and IRG were increased markedly in amino acids infusion.

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D-Xylose absorption test has been used for the measure of intestinal absorption of carbohydrate. The oral dose of 5g or 25g has been employed traditionally in the D-xylose absorption test. We have investigated this problem of dose in clinical study. It has been revealed that urinary excretion of D-xylose reaches the maximum at dose of 25g, and does not increase any more with further more increasing dose of D-xylose. This finding indicates that the dose of 25g brings to intestinal concentration of D-xylose absorbed maximally.
Consequently, the authors consider that the dose of 25g will give a more thorough test of absorption from the small bowel.

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In the D-xylose absorption test, the amount or rate of D-xylose excreted in urine decreases with increasing age. It has been still debated whether its reduction is due to impaired intestinal absorption or to deterioration in renal function.
We have investigated this problem by in vitro study using jejunal everted sacs of rats and clinical studies consisting of the D-xylose test (25g orally) to 44 subjects, the creatinine clearance to detect renal function in elderly, and the intravenous D-xylose test for correcting of the D-xylose absorption test.
These studies show that the diminishing D-xylose excretion in elderly is due to the depression of renal function mainly glomerular filtration rather than to impaired intestinal absorption.
Furthermore, we propose the corrected normal value of the D-xylose absorption test (25g orally) as follow; 5.9 to 9.1g (23.4 to 36.4%) in young (under 50 y.o.) and 3.7 to 6.0g (15.0 to 23.8%) in elderly (over 50 y.o.).

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Serum protein binding form of Indocyanine green (ICG) was examined by the following methods; starch block electrophoresis using the ICG labeled serum, immunoelectrophoresis and electrofocussing fractionations.
Large peak of the ICG binding form in albumin fraction and small peak of the ICG binding form in β-globulin fraction were observed by starch block electrophoresis.
These fractional extracts were subdivided by gel filtration in Sephadex G-200, and then were analyzed using immuno-electrophoresis. Major peak mainly consisted from α₁-lipoprotein (a₁-LP) and minor peak consisted from β-lipoprotein (β-Lp), also same results were obtained from the method of electrofocussing fractionations.
From these results, ICG bound mainly to a₁-Lp and β-Lp, but bound scarcely to albumin and might be have a poor affinity.

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It is said that peptic ulcer is frequently combined with liver cirrhosis. But reason for this phenomenon remains unexplained in spite of many theories. To explore it, we studied 91 cirrhotic patients diagnosed by laparoscopy with histological confirmation or autopsy from Jan. 1968 to Dec. 1973.
All of these patients were examined thier upper gastrointestinal tract endoscopically, and peptic ulcer was found in 13 patients (14.3%). These included 7 chronic gastric ulcers, 2 duodenal ulcers, 2 gastric and duodenal ulcers, and 2 acute gastric ulcers. Characters of these ulcers were almost the same as ordinary ulcers uncombined with liver cirrhosis.
To investigate causes of ulcers in cirrhotic patients, we studied acidity of gastric juice, serum gastrin level, grade of esophageal varices and splenomegaly, and pressure of the rectal veins. As in the gastric acidity, patients with ulcer had a tendency to be only slightly higher gastric acidity than those without ulcer, while almost all patients showed normoacidity. Serum gastrin level in ulcer patients was almost the same as in patients without ulcer. Grade of esophageal varices, splenomegaly and rectal venous pressure which we adopted as the indicators of severity of portal hypertention were not so different between ulcer and nonulcer groups. There was no great difference in the presence of history of acute hepatitis, blood transfusion and grade of alcohol intake between both group. As for the relation to the patterns of liver cirrhosis, we could not obtain any clear result because it was very difficult to classify the patterns of liver cirrhosis only with laparoscopy and liver biopsy, and there were only few cases of autopsy in this series.
Healing course of peptic ulcer is relatively rapid, on the contrary, liver cirrhosis has a slow and progressive course. We could not find out any significant relationship between healing or recurrence of gastric ulcer and the activity of liver cirrhosis in this small series.
Massive upper GI bleeding occured in 25 cases in our series (28.6%). The sources of bleeding were 3 gastric ulcers, 2 duodenal ulcers and 2 esophageal varices in ulcer group, on the contrary, all those of the other 18 patients were from esophageal varices in non-ulcer group.

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A 60-year-old man was admitted to Okayama University Medical School with a 2-month history of vomiting and weightloss, and with a palpated abdominal tumor and hyperamylasemia (1, 650 Somogyi unit). Laparotomy underwent because of mechanical obstruction caused by the colonic tumor, whose histology revealed undifferentiated adenocarcinoma. Serum and urinary amylase levels remained abnormally high during 7 weeks' admission. The amylase activity in a metastatic tumor tissue on the omentum was over ten times higher than those in serum and ascitic fluid. Ion exchange chromatography disclosed that the elution patterns of amylase in the serum, ascites and tumor tissue resembled that of salivary amylase. Electron microscopic studies showed that each tumor cell is in close contact with neighboring ones and has a tendency to form small nests, suggestive of undifferentiated adenocarcinoma. Zymogen-like granule was not observed in this case.
Data obtained suggests that the 'S' type amylase might be produced ectopically by the tumor tissue.

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