Intra-hepatic vascular changes following ligatation of the common bile duct in the male rats, were studied at the 1, 2, 5 and 10th week periods after the operations. Histologically, the parenchymal cell degeneration in the centrolobular areas was observed on the 2nd day after the operations and proliferation of the intralobular bile ductules was seen in the periolobular areas at the 2nd week after the operations. Proliferated bile ductules in the portal triads were accompanied with proliferation of connective tissues and tended to surround the lobules at the 5th week. In a few cases of the 10th week group, histological features compatible with biliary cirrhosis were observed. Proliferation of connective tissues began mainly in the portal areas and partly in the central areas. Recognizable alteration of the intra-hepatic vessels was not observed at the 1st week period. At the 2nd week period, the terminal branches of the portal veins showed slight proliferation and distortion. After the 5th week of the experiments, the livers revealed marked dilatation and tortuosity of the large hepatic arteries, and distinct proliferation of the tortuous small or middle arteries. In some arteries of middle size, abrupt obliteration in a segmental fashion was observed. Prominent distortion and proliferation were seen in the portal veins of small to middle size, and porto-portal anastomoses were found in the vessels of middle size. On the other hand, the hepatic vein showed no recognizable alteration, except slight distortion in a few cases which showed pre-cirrhotic features. It was suggested that these vascular changes may be due to compression of vessels by the proliferated and dilated bile ductules. The intra-hepatic vascular alterations in obstructive jaundice were completely different from the features in liver injury induced by choline deficiency or CCl4 administration.
Incomplete treatment of gastric ulcer or the state being accustomed to such treatment are probably the responsibility of both the side of conducting treatment and the side of patient. The actual state of autopsied and clinical cases as well as clinical findings to be used as the reference of therapeutic program were analyzed. 1. From the autopsy records of Tokyo Medical Examiner's Office, the death rate due to gastric ulcer was found to be decreased but the gastric ulcer as a side change was not decreased. The rate in gastric ulcer was decreased in recent years. 2. In clinical cases, the patients start to fall out from the stage of diagnosis. Only 30% of patients who were treated were confirmed as being healed after 1 year. 3. Upon studying the course of ulcer in hospitalized and out-patients separately, ulcers in hospitalized patients are large and appear to resist treatment while ulcers in out-patients are small and appear to be cured readily. However, the tendency to healing was less in outpatients. 4. Depend on the depth of the ulcer influences the responsiveness to treatment, attempts to predict the depth of the ulcer were made. The rate of correct prediction in the prediction of UL IV was as high as 85%, while the corresponding value in UL III was only 25%. Most of the ulcers predicted as UL III were actually deeper.
Based on the reasoning that the incompleteness in the treatment of gastric ulcer reported previously is based on the vagueness of the decision of therapeutic principle and the general rule that the treatment of gastric ulcer should be medical, a brief trial of rigid medical management was examined as the starting point. 1. The object is the diagnosis through treatment to differentiate between benign and malignant lesions and between those which respond readily to treatment and those which do not. 2. Using the Bockus-Paustian's original method as the reference, 2 weeks of non-irritating fluid diet such as milk, rice soup, juice, soup and bean-curds were prescribed. 3. Changes in the result of general clinical tests before and after this treatment were not remarkable except for elevation of gastric ulcer. 4. In 34 cases or 60%, reaction to treatment was favorable with decrease in the size of the ulcer, while no decrease in size was noted in 23 cases or 40%. However, it is difficult to predict the results of therapy from the clinical findings before treatment. 5. In patients who responded favorable to treatment, the subsequent course was good, resulting in the rate of healing of 82% after 1-3 years of following up period. In those who responded poorly to treatment, only 15% reacted the state of cure, showing a distinct difference. 6. No decrease in size was seen in malignant ulcer. As a method of diagnosis through treatment, this brief trial of rigid medical management seems to be reasonable.
There has been no agreement in opinions as to whether the fibrogenetic process in the liver with extrahepatic obstructive jaundice starts from the portal triads or the pericentral areas of hepatic lobules. In order to study the fibrogenesis of biliary cirrhosis, histological studies were carried out on liver specimens obtained by needle biopsy, laparotomy or autopsy in 46 cases (calculosis of the bile duct, 11; carcinoma of the head of the pancreas, 10; carcinoma of the bile duct, 17 and miscellaneous, 8). Among these 46 cases, no fibrotic change was revealed in 16 (34.8%), slight fibrosis in 12 (26.1%), considerable degree of fibrosis in 13 (28.3%) and definite pictures of biliary cirrhosis in 5 (10.9%), respectively. Mean durations of jaundice due to the extrahepatic obstruction in each group was 40.3±9.3, 87.2±33.2, 181.2±44.2 and 873.6 days, respectively. There were no relations between the degree or site of obstruction in the bile duct and the degree of fibrosis of the liver. Histological observation revealed that the degree of fibrosis of the liver correlated with the degree of bile ductular proliferation, but did not correlate with the degree of parenchymal necrosis, bile stasis or proliferation of inflammatory cells. Concerning the fibrogenesis of the liver in extrahepatic obstructive jaundice, fibrosis began mainly from the periportal areas, and in a few cases it began from the centrolobular areas. In some cases, the two patterns of fibrosis coexisted more or less intermingling with other. At the early stage of obstruction, slight fibrosis of the liver was predominantly found in the portal and perihepatocellular areas. As the fibrosis progressed, periductular fibrosis became prominent. Serial microscopic examination of the liver specimens revealed that fibrous bands originated from the periportal and/or intralobular areas accompanying with marked bile ductular proliferation mainly connected with the fibrous bands in the neighboring portal triads. And partly, they also connected with the small fibrotic strings around central veins caused by parenchymal degeneration. It was assumed that these connections of the fibrous bands might gradually divide hepatic lobules into small pseudolobules.