The present paper deals with the secretory function and the emptying of the stomach in cases with peptic ulcer, observed using telemetering pH capsules and phenol red test meal method. 1. The alkali time was shortened and the emptying was accelerated in cases of duodenal ulcer, and vice versa in cases of gastric ulcer. The difference between the two diseases was statistically significant (p=0.05), although the difference from those of the healthy controls was not significant. After the disappearance of the niche of ulcer, the emptying became delayed in duodenal ulcer, and accelerated in gastric ulcer, compared to those before treatment. 2. The effect of the various foods on the secretion and emptying was observed by means of phenol-red test meal method. The delay of the emptying was seen with glucose solutions (10%, 20%-180ml), and the inhibition of both functions was detected with olieve oil (5%, 10%-180ml). The starch and the egg white showed no definite inclination. 3. The in vitro neutralizing capacity of the various foods was proved to be dependent on those protein content. The in vivo antacid effect of the foods was also predominantly influenced by those protein content. The significance of the abnormal motility concerning the pathogenesis and the healing of the ulcer was discussed, together with the problem of the intragastric pH in the treatment of the ulcer.
The fluid aspirated from the jejunum and ileum in 11 non-hepatic and 19 hepatic diseased patients was incubated both aerobically and anaerobically (Steel-Wool Method). 1) The flora found in the jejunum and ileum of the hepatic diseased patients frequently (Ca.50%) contained non-spore forming gram positive rods such as Corynebacterium and Eubacterium with anaerobic cocci, whereas the jejunum of the non-hepatic diseased was mostly free from anaerobes except few cases with anaerobic cocci such as. Peptococcus, Peptostreptococcus and Veillonella. 2) The ratio between rods and cocci in anaerobes was about 56% to 44% in the small intestine of the hepatic diseased, whereas cocci is overwhelming in the non-hepatic diseased cases. 3) The average count of anaerobes in 0.5ml of intestinal juice was 103.9 in non-hepatic diseased jejunum, whereas 105.5 in hepatic diseased jejunum. On the other hand, 105.9 in hepatic diseased ileum. 4) Anaerobic gram positive rods such as Corynebacterium and Eubacterium were found in; 0% in subjects with gastric juice under pH 4, whereas 55.4% over pH 4. They also were found in abnormal subjects in liver function tests such as A/G, T.T.T., Z.T.T. and Alkaliphosphatase reaction twice as much as normal subjects. 5) Anaerobes isolated from the small intestine are highly sensitive to various bile acids such as sodium cholate desoxycholic acid, sodium taurocholate and sodium glycocholate, compared with aerobes.
In order to investigate the pathogenicity of the non-spore forming anaerobe, we inoculated mice (15g) intraperitoneally with various dilutions of normal saline suspensions of non-spore forming anaerobes isolated chiefly from gallbladder, and LD50 was calculated in colony count respectively. Each mouse was autopsied and investigated pathologically. The same procedures were done with aerobes. 1) LD50s of various species of anaerobic rods were as follows: 109.9 of Eubacterium (3 strains), 1011.0 of Corynebacterium (4 strains out of 6) and 1012.4 of Ramibacterium (1 strain). With regard to cocci, LD50s were obtained in only 3 strains out of 8; 108.6 of Peptostreptococcus intermedius (1 strain), 1011.5 of Peptococcus (1 strain), 1011.6 of Veillonella (1 strain). On the other hand, LD50s of aerobes were as follows; 1010.0 of E. Colli (3 strains), 1010.8 of Staphylococcus aureus (3 strains), and 107.4 of β-streptococcus (3 strains). 2) Although vilurence of the anaerobes is inferior to that of the aerobes in general, there are many strains that are equal or superior to pathogenic aerobes in vilurence, such as whole strains of Eubacterium, many strains of Corynebacterium and some strains of Peptostreptococcus. 3) The pathological examination of the experimentally infected mice revealed the followings: In the dead mice group, severe degree of pathological change such as perisplenitis, perisplenal abscess, liver abscess and peritonitis were observed in general. On the other hand, in the survived mice group, pathological changes were slight. It is concluded that many strains of the anaerobes have strong vilurence and pathogenicity.
Although a considerable number of works have been done, the etiological mechanism and distribution of pancreatitic lesions are not fully understood. The present paper deals with the pathological changes in pancreas taken from 108 cadavers and the influence of peritoneal lesions upon pancreas. In addition, radiological examination of normal vascular and ductal systems was also investigated. And the following results were obtained: 1. Lobular atrophy, necrosis and fibrosis seemed to have been caused by the circulatory disturbance at the level of intralobular artery which was functinal end-artery though abundunt anastomoses were confirmed in its proximal portion. Systemic circulatory disturbance caused acinar atrophy followed by sporadic fatty replacement, which was exceptionally developed to the severe and extented lesion. Pseudo-lobulation in pancreas was seemingly due to venous congestion. 2. Ductal obstruction in each segment, caused pathologic lesions in its corresponding area; fat necrosis and focal fibrosis were frequently developed in the peripheral region of pancreas in which abundant ductules were radiologically confirmed. Periductal circumscribed necrosis and cellular infiltration suggested the leakage of pancreatic juice due to ductal obstruction. 3. Ascites, especially purulent one, would bring pancreatic edema, cellular infiltration and fat necrosis. The inflammatory changes were advanced to superficial parenchymal necrosis in severe peritonitis. It should be noticed, therefore, that anatomical correlation between pancreas and peritoneum plays important role in this type of pancreatic lesion. 4. These lesions in vascular or ductal origin and from surrounding tissue might be influenced one another and developed to such a severe change as hemorrhagic necrosis.
A study was made on tetrachloride induced-cirrhotic rats with ascites as well as on normal rats to study the mechanism of ascites absorption from the peritoneal cavity. 1) In normal rats, parasternal lympf vessels and a vessel along the right phrenic nerve were clearly demonstrated in X-ray films following peritoneal injection of Thorotrast. In the rats in which the parasternal lymph vessels had been ligated, the appearance in serum of radioactive goldcolloids infused into the peritoneal cavity, was significantly delayed. These findings suggest that the parasternal lymph vessels are the main route for the lymphatic drainage from the peritoneal cavity to the greater circulation. 2) In the X-ray study of the cirrhotic rats with ascites, the thoracic duct was clearly visualized after intraperitoneal injection of Thorotrast in addition to the mediastinal lymph vessels, suggesting that the thoracic duct plays also an important role in the drainage of ascites in cirrhosis. 3) The appearance in serum and the uptake into the liver, kidney and spleen, of radioactive gold colloids, infused into the peritoneal cavity, were greater in cirrhotic rats than in normal rats. 4) The thoracic lymph volume and the appearance in the thoracic lymph of radioactive gold colloids or 131I-albumin, infused into the peritoneal cavity, were greater in cirrhotic rats with ascites than in normal rats. 5) The study with electoron microscopy revealed that the gold colloid particles, infused into the peritoneal cavity, were pinocytosed into the mesothelial cells and drained into the lymph vessels of the diaphragm within five minutes of infusion. In cirrhotic rats with ascites, the mesothelial cells of the peritoneum appeared to be thicker and have more pinocytic vesicles. These findings seem to indicate that, in cirrhotic rats with ascites, the peritoneum becomes more active in the removal of colloid particles in ascites and their carrier ascitic fluid.
II Chronological degeneration of the exfoliated gastric cells. Degeneration of the human exfoliated gastric cells was chronologically studied and its difference in each disease was found. (1) The cells from the normal lining epithelium showed the most rapid degeneration, followed by what appeared to be regenerating epithelial cells from ulcer and polyp, and the malignant cells from the marginal areas of advanced cancer showed the longest survival. (2) The cells from the type IIc of early carcinoma presented similar degenerative process to the regenerating epithelium. (3) In the benign cells, degeneration of the nucleus and cytoplasm start at the same time, whereas in the cell from advanced carcinoma nuclear degeneration preceeds. (4) Karyolysis is ordinarily completed prior to destruction of the cytoplasm. (5) The cells from the central portion of advanced cancer show a marked difference in the speed of degeneration in comparison with the cells from the margins. This was probably due to the nutritional difference, which was proved by an experiment.