Nippon Shokakibyo Gakkai Zasshi
Online ISSN : 1349-7693
Print ISSN : 0446-6586
Volume 69 , Issue 5
Showing 1-7 articles out of 7 articles from the selected issue
  • Masaharu TATSUTA
    1972 Volume 69 Issue 5 Pages 459-473
    Published: May 05, 1972
    Released: June 17, 2011
    JOURNALS FREE ACCESS
    An endoscopical examination method of gastritis in upper portion of the stomach and the map of cardiac gland area was demonstrated by the congo-red test which indicates acid secreting function in detail, and their clinico-pathological studies were made by the biopsic specimen and/or resected stomach.
    1) Histological survey on the 20 resected human stomach revealed that cardiac gland area was recognized in only 50%, and even in the 50%, cardiac glands were confined within extremely narrow area of which average was 2 mm from esophago-gastric junction, up to where the fundic gland area occupied in many instances.
    2) By means of the congo-red test, extent of gastritis in upper portion of the stomach can be easily observed endoscopically as “non-discolored area” that has no acid secreting function. The pattern was divided into the following 3 types;
    a: Whole sight around cardia is the discolored area by sound acid secretion for absence of gastritis.
    b: Co-existence of discolored and non-discolored area by partially impaired acid secretion for partial gastritis.
    c: Entire impairment of acid secretion due to pan-gastritis.
    3) Histological findings in gastritis of the upper portion of the stomach were mainly atrophy of fundic glands and intestinal meta plasia. Epithelial defect, edem, infiltration of inflammatory cells and hyperemia were also seen.
    4) In the way of gastritic extention, besides (1) from the lower corpus to the cardia, there is another way (2) that begins in the cardia and spreads to the lower.
    5) Gastritis which begins from cardiac side, grows with aging, and the histological changes were advance of fundic glands' atrophy and intestinal metaplasia.
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  • Kose SEGAWA
    1972 Volume 69 Issue 5 Pages 474-490
    Published: May 05, 1972
    Released: June 17, 2011
    JOURNALS FREE ACCESS
    The gastro-duodenal ulcer was produced in rat through the intravenous administration of gastrin-tetrapeptide. Its ulcerogenesity was decreased by the gastro-intestinal hormones, secretin and gastrone-like substance. To disclose the mechanism of gastrin-ulcerogenesis and the inhibitory mechanism by secretin and gastrone, the activity of gastrin and the effect of secretin and gastrone were studied as regard to acid-output, pepsin secretion, duodenal motility and parietal cell formation.
    The secretin was extracted from the hog duodenum at Eisai, Ltd.(Tokyo). The gastrone was the glyco-peptide extracted from the whale at Nissui Seiyaku, Ltd., (Tokyo).
    The followings are the results:
    1) The duodenal ulcer was produced at the rate of 60% by intravenous administration of gastrin (100γ/kg-h.) for 12 hours. The admixture of secretin (8 U/kg-h.) or gastrone (960γ/kg-h.) lowered the ulcerogenesity to the rate of 20%.
    2) In the group administered with gastrin the mean acid out-put for 6 hours amounted to 0.532±0.0708 mEq; 0.1082±0.0148 mEq in gastrin and secretin; 0.0968±0.0189 mEq in gastrin and gastrone. The number of each experiment was 6.
    3) The peptic output for 6 hours amounted to 13.69±59 tyrosine mg in the group administered with gastrin; 16.82±1.09 tyr. mg in gastrin and secretin; 14.05±1.22 tyr. mg in gastrin and gastrone and 7.04±0.60 tyr. mg in control group. The statistically significant difference exists between gastrin group and control group; gastrin group and‘gastin +secretin’group.
    4) The duodenal motility was activated slightly by gastrin compared with saline. The gastrin activity was inhibited by secretin and gastrone above mentioned. The inhibitory activity of gastrone was stronger than secretin.
    5) The number of the parietal cell and the height of mucous membrane at the fundic area of rats, which were administered with gastrin solved in 16.6% gelatin for 30 days, increased as compared with control group administered with 16.6% gelatin for the same period. This activity was, also, reduced by secretin (8U) or gastrone (960γ) similarly.
    From the data above mentioned the author supposes that the gastro-intestinal hormones may play the important role in the ulcerogenesis.
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  • Yukiyoshi KAMISAKA
    1972 Volume 69 Issue 5 Pages 491-502
    Published: May 05, 1972
    Released: June 17, 2011
    JOURNALS FREE ACCESS
    Despite extensive research works, the mechanism of choleraic diarrhea is still in dispute. The rapid increase in knowledge of biologic effects of cholera enterotoxin has risen the possibility that increased vascular and mucosal permeability and/or cyclic AMP are contributing to rapid loss from the gut of an isotonic fluid. Cholera enterotoxin discernibly increased the permeability of the microcirculatory system of the rat mesentery when given intravenously or applied locally and gave rise to degranulation of the mast cells around the vessels. Electronmicroscopic study of the vessel wall with increased permeability disclosed separation of endothelial junctions without any other ultrastructural change. When marker particles were used, these particles were observable in endothelial junctional sites and outside of the basement membrane. Furthermore, there was the endothelial cytoplasm having pinocytotic vesicles. Ethacrynic acid, cycloheximide, prednisolone and chlorpromazine interfered with effects of the toxin, resulting in unaltered permeability of the vessel. When rats were premedicated by those pharmacological agents, the enterotoxin failed to degranulate the mast cells. The present study suggests that one of the primary target of cholera enterotoxin is the increased permeability of the blood vessel by direct effect of the toxin and degranulation of the mast cell.
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  • Kagemitsu KATO
    1972 Volume 69 Issue 5 Pages 503-523
    Published: May 05, 1972
    Released: June 17, 2011
    JOURNALS FREE ACCESS
    In order to provide a basis for the interpretation of pancreatograms, the relation of radiological findings of the pancreatic duct system to histological findings were studied in 84 necropsy materials, including 14 cases of carcinomatous lesions in the pancreas.
    The results were as follows:
    1. The course of the main pancreatic duct were classified into four types and that of the accessory duct into three types. By giving these types careful embryological consideration, comprehensive understanding of these complicated courses of the ductal system is relatively easy.
    2. A correlation was shown between the type of the ductal course and the form of opening into duodenum, concerning the main and accessory pancreatic, and bile ducts. The form of ductal opening seemed to play an important role to the possible disturbance of pancreatic function due to the pathological changes of ampulla region.
    3. The mean maximum diameter of the main duct in 21 cases with abnormal histological finding in the pancreatic parenchyma was bigger than that in 49 normal cases but the caliber of the main duct was found to increase with age and to have remarkable variation in each individual case.
    4. Narrowing of the main duct in the neck of the pancreas and the constriction immediately above the Vaterian pancreatic duct appeared to exist in normal cases.
    5. Sparse ramification of ductal system in the neck of the gland seemed to be in connection with aging.
    6. The diameter of the branches bigger than 1mm except the chief ones, the wavy contour of the branches and the beads-like or cystic dilatation of the branches were all closely related to the hyperplastic or metaplastic changes in the ductal epithelium and the inspissated mucinous materials in the duct.
    7. In carcinomatous lesions of the pancreas, general findings were the stenosis or obstruction with rigid outline of the main duct and interruption and straightening of the branches. Above the constricted part of the duct was seen the secondary dilatation of ductal systems.
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  • 1972 Volume 69 Issue 5 Pages 524-556
    Published: May 05, 1972
    Released: June 17, 2011
    JOURNALS FREE ACCESS
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  • 1972 Volume 69 Issue 5 Pages 557-575
    Published: May 05, 1972
    Released: June 17, 2011
    JOURNALS FREE ACCESS
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  • 1972 Volume 69 Issue 5 Pages 576-582
    Published: May 05, 1972
    Released: June 17, 2011
    JOURNALS FREE ACCESS
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