The gastric mucosa was obtained from the corpus of the stomach of 74 patients by suction biopsy under fluoroscopy before and 45 minutes after histalog injection at the dose of 1.5mg/kg. The gastric acid secretion, histological appearance of gastric mucosa and fine structure of the parietal cells was observed in order to investigate the function of the parietal cells in chronic gastritis. The results was as follows: 1) The gastric acid secretion was decreased, and it appesrs to be due to the atrophy of mucosa, the cellular infiltration in the lamina propria and the sclerosis of tunica muscularis mucosa either before or after histalog stimulation. 2) Remarkable changes in morphology of mitochondria, intracellular canaliculi and microvilli after histalog which were seen in normal cases were not found in hyposecretion. 3) Mitochondrial swelling, the development of the intracellular canaliculi and microvilli were found inhibited in the atrophy of gastric mucosa, but in the cellular infiltration in the lamina propria and the sclerosis of tunica muscularis mucosa, the latter was not significantly inhibited. From the above, the cellular infiltration in the lamina propria and the sclerosis of tunica muscularis mucosa slightly influence on the structure of the parietal cells as compared with the atrophy of gastric mucosa. 4) The mitochondrial swelling was remarkable after histalog stimulation. The observation of the mitochondrial morphology is important on the study of the function of thegastric parietal cells. The resting and secretive findings were seen before histalog but only secretive findings of the parietal cells were found after histalog. On the fine structure of the parietal cells in atrophic gastritis, the mitochondria were large in size as compared with normal cases in resting state. But the mitochondria did not became so large in size after histalog as in normal cases and intracellular canaliculi and microvilli did not develop. In superficial gastritis, the mitochondria were large in size before histalog but smaller in size in secretive state than in normal cases. Therfore, the mitochondrial swelling were not remarkable but intracellular canaliculi and microvilli well developed in superficial gastritis.
16 kinds of enzymes were cytochemically examined for the purpose of application to cytochemical diagnosis of gastric cancer. They are Alkaline phosphatase (ALP), Acid phosphatase, Leucine aminopaptidase (LAP), Esterase, 5'-Nucleotidase, β-Glucuronidase, phosphorylase (PR), Lactic dehydrogenase, Malic dehydrogenase, Glutamic dehydrogenase, Succinic dehydrogenase, Glucose-6-phosphate dehydrogenase, lsocitrate dehydrogenase, NADdiaphorase (NADd) and Monoamine Oxidase. The resutts show efficiency of combined methods of three enzymatic staining, LAP, ALP and NADd, as well as PR. This finding was applied to the cytology of 100 cases of gastric cancer. Both cytochemical and cytomorphological diagnosis compensate each weak point's with total diagnostic results attaining to 100%.
In an attempt to study the mechanism underlying for the impaired glucose tolerance in liver disease, 1) changes in serum IRI levels in response to oral glucose (50g) and 2) the effect of exogenous insulin (0.1U/kg, i.v.) on blood glucose levels were examined in patients with various liver diseases (acute and chronic hepatitis and liver cirrhosis). In some of these patients, IRI response to oral glucose was repeatedly (twice or more times) examined at intervals of 3 to 6 months. In addition, IRI levels following intravenous glucose (25g) and those following intravenous tolbutamide (1g) were also determined in cirrhotics. Subjects with no evidence of either liver disease or diabetes mellitus served as controls. Results are summarized as follows: 1) Patterns of IRI response to oral glucose were classified into 5 types; namely, a) normal response, b) delayed normal response, c) hyperresponse, d) delayed hyperresponse and e) hyporesponse types, respectively. 2) In a large number of patients with liver disease, IRI response to oral glucose was either normal or hyperresponsive, including delayed response of both types. Mean values for IRI at 30, 60, 90 and 120min. after glucose load in liver diseases were all significantly higher than those in controls. 3) In most of the patients with acute hepatitis, IRI response to oral glucose examined within a month of the onset was hyperresponsive. However, after hepatitis was recovered, the IRI response returned to normal in all of the patients. In cirrhotics, the IRI response was hyperresponsive in a half of them and normal in the remainder. However, the IRI response re-examined 3 to 9 months later was found to be hyperresponsive in all of the patients. In patients with chronic hepatitis, follow-up sutides of IRI response did not show any definite tendency as observed in previous two groups. 4) Sensitivity to the exogenous insulin in liver disease was significantly diminished, suggesting that insulin demand to utilize glucose in the peripheral tissue was augmented in liver disease as compared with that in controls. Thus, insulin output from the Langerhans' islet cell would be compensatorily increased in liver disease. 5) IRI levels following intravenous glucose and those following intravenous tolbutamide, in cirrhotics, were also significantly higher compared to those in controls. These findings indicated that the output of insulin in liver disease could be acceralated after glucose load even without any actions of intestinal hormons such as secretin.
Acute massive hemorrhage from the upper alimentary tract is usually caused by gastric or duodenal ulcer, gastric cancer, esophageal varices, and Mallory Weiss syndrome. The author has treated 93 cases of acute massive hemorrhage caused by gastric and duodenal diseases. They include one case of Exulceratio simplex (Dieulafoy) and 17 cases of gastritis. These two conditions are relatively rare cause of acute massive hemorrhage and must be treated in different approaches. Exulceratio simplex (Dieulafoy), reported by Dieulafoy in 1897, is characterized by a rupture of the varix in gastric wall. The varix is commonly located at the upper part of the stomach and unable to be detected by a palpation of the stomach. Therefore, blind gastrectomy is not effective and could rather be lethal surgery for this disease. The most resonable treatment is to open the stomach, and ligate the bleeding vessel or excise the bleeding area. Massive hemorrhage by gastritis is more common, and characterized by desquamation of the epithelium of gastric mucosa which is accompanied by acute catarrhal inflammation and reactive hyperemia. The mechanism of the bleeding would be supposed a capillary bleeding from the desquamated area. As the treatment of this disease, the author recommends partial blind gastrectomy of the antrum. All of the 17 cases were completely healed by this treatment.