In order to analyse the important factors of gastric juice as the cause of the primary esophagitis, the experimental esophagitis was observed 8 hours after the injection of 0.1ml of the Shay's rat or artificial gastric juice into rat esophagus ligated at the upper and lower end. The incidence of esophagitis was increased dependent upon the duration after administration of gastric juice. When the gastric juice was diluted from 5/6 to 1/6 times, the incidence was almost related to the concentration of gastric juice. Likewise, an artificial gastric juice was administered. Esophagitis was not caused by a pepsindeficient artificial gastric juice of pH 1.5, 1.8, 2.0 and 2.2, respectively. However, artificial gastric juice containing pepsin at similar concentrations as diluted rat gastric juice caused esophagitis as often as the diluted gastric juice. After the application of artificial gastric juice with pH 1.5, 1.8 and 2.0, each containing pepsin at the concentration of 20, 10, 6.7 and 3.3mg/ml, the incidence of esophagitis was high even at pH 2.0, when the concentration of pepsin was high. However, when the concentration of pepsin was low, its incidence was much influenced by the concentration of pH. The rat gastric juice, which was corrected to pH 1.5 after pepsin was inactivated by alkalization, could not cause esophagitis. The rat gastric juice containing basic sodium sucrose sulfate at the concentration of 100, 60 and 40mg/ml, respectively, failed to cause esophagitis. However, esophagitis developed in 20% of animal when 20 and 10mg/ml of this salt was administered, and also the same pathological findings were seen in 60% of animal with the use of 5mg/ml of this salt. Foregoing findings suggest that the incidence of esophagitis increases as pH of the gastric juice becomes lower and as the concentration of pepsin becomes higher. The concentration of pepsin was considered to be more important than the degree of pH.
Clinical and pathological findings were reported on three cases of ulcerative colitis. On microscopic examination, cryptitis and cryptabscess were observed in early lesion of the disease, and subsequent formation of ulcer was seen, having granulation tissue with numerous plasma cells and abundant vascularization in the base of it. Regeneration of mucous membrane, proliferation of edematous connective tissue and formation of pseudopolyposis ensued. These pathological processes were characteristic of this disease, and always repeatedly occurred. There were neither vasculitis as a cause of ulcerative colitis which was described by Warren and Sommers et al. nor atrophic change of mucous membrane described by Matsunaga et al. in our three cases.
The mesenchymal areas stained in blue and the parenchymal areas stained in purple in the staining sections of the liver specimens with azan were estimated in 17 patients of subacute hepatitis diagnosed according to the criteria of Tisdale. The ratios of two areas (M/P) or of the mesenchymal areas to the total areas (M/T) were calculated to evaluate the volume of hepatocellular destruction. The relation between the area ratios and the clinical features. was also studied. Variations in the estimated values of the M/P or M/T ratios in any depth of the biopsy specimens or in any part of liver in the autopsy cases were very small in each case, indicating that the estimated values in any section may reflect the quantitative changes of hepatocellular damage throughout the entire liver. The values of the M/P (M/T) ratios in subacute hepatitis were all above 0.21 (17.3%), and were significantly higher than those in acute hepatitis. or chronic hepatitis including active form. The M/P (M/T) ratios of the patients died of hepatic coma were all above 2.52 (71.6%) and were significantly higher than those of the survived cases. Severe clinical signs, such as prolonged jaundice, ascites, edema, neurological findings and gastrointestinal bleeding tended to be found more frequently in the cases showing the larger M/P (M/T) ratios among the survived cases. However, the development of hepatic cirrhosis was not correlated to the area. ratios in the initial biopsy specimens. The results indicated that subacute hepatitis was clearly differentiated from acute or chronic hepatitis by the quantitative evaluation of the mesenchymal area. And the quantity of the initial destruction in the hepatocytes was closely related to the fatality or the developments of the severe clinical signs in the relatively early stage. However, the prognosis in the late stage, which means development of hepatic cirrhosis, may be influenced by the reaction in the host following the hepatocytic destruction rather than the quantity of the hepatocellular damage.
The lactic dehydrogenase (LDH) activity and its isozyme pattern was determined in the serum, liver and cancer tissue of rats with experimental metastatic cancer of the liver produced by transplantation of ascites hepatoma AH66F into the spleen and in patients with metastatic cancer of the liver. The following results were obtained. 1) The LDH activity in the serum of rats with AH66F metastatic cancer of the liver increased significantly as compared with the control. The same result was obtained in the serum of the patients with metastatic cancer of the liver. 2) In LDH isozymes in the serum, LDH-4 was found to have increased with progression of liver metastasis in the rats with AH66F metastatic cancer of the liver. 3) The LDH activity of cancer tissue in rats with AH66F metastatic cancer of the liver decreased as compared to the control liver tissue. The same result was also obtained in the cancer tissue of patients with metastatic cancer of the liver. The LDH isozyme pattern of non-cancerous tissue in rats with AH66F metastatic cancer of the liver also had a tendency to be similar to that of the cancer tissue. 4) In LDH isozymes in the serum, LDH-4 and LDH-5, especially LDH-4 was found to have increased in patients with metastatic cancer of the liver, and the cases with LDH-4> LDH-5 were observed in 73% of the patients with metastatic cancer of the liver. 5) Therefore, the determination of LDH activity and its isozyme pattern in the serum is thought to be useful in the diagnosis of metastatic cancer of the liver.
Ioslated homo- or hetero-logous liver perfusion is being used in the treatment of hepatic failure which may provide temporary support for the patients. The present study is subjected to decide an optimal condition for liver perfusion and a liver function under cooled preservation using laboratory animals, and resulted in the followings: 1) From these data of liver function tests, rate of bile outflow, liver outflow block and liver oxygen consumption, two systemic perfusions of portal vein and hepatic artery are need to perfuse the liver with volume rate at 0.5-1.0ml. per gram of liver per minute. 2) Perfused liver to preserve under 4 degree C. showed no remarkable changes on histological and functional examinations within six hours. 3) Perfusions of fresh liver and cooled preserved liver did well and resulted in successful for the treatment of experimental hepatic failure. This method could improve the general condition of the animals and not find any functional differences between fresh liver and cooled preserved liver.