In order to clarify that which subcellular fraction of the damaged liver may play a major role for the hepatic fibrosis, the incorporation of C14-proline and its conversion to hydroxyproline were examined at the early stages of the experimental liver injury on the separated hepatocytes prepared by a sucrose gradient centrifugation. It was found that the radioactive proline and hydroxyproline are readily significant in the microsomal fraction of hepatocytes at the early stage of the liver damage, and then their marked incorporations are transfered to the soluble fraction in the later stage of the liver damage. The antifibrogenetic effects of cortisone, 4-aminoproline, p-carboxyphenylglycylaminoacetonitrile, and 6-mercaptopurine were examined on the fibrogenetic process of the liver injury and found that they have an inhibitory effect on the incorporation of proline and its hydroxylation in the ribosomes of the hepatocytes, while 6-mercaptopurine has a marked suppressive effect on the formation of both collagenous and non-collagenous protein.
Studies were pursued on the mechanism of an inhibitory effect of polysulfated glycopeptide (GLPS) extracted from hog intestinal mucosa on the proteolysis of albumin substrate. In agar gel plate, precipitation reaction was observed between GLPS and albumin substrate, but there was no precipitation reaction among pepsin, N-acetyl-phenylalanyl-diiodotyrosine and GLPS. In condition of a constant quantity of albumin substrate and of GLPS, variation of pepsin concentration did not affect the proteolytic inhibition rate of GLPS. In certain range of GLPS concentration, proteolytic inhibition was dependent on albumin concentration, however, the quantity of substrate protected by a given amount of GLPS was independent of the concentration of the substrate and of GLPS. It was assumed that the mechanism of the inhibition of peptic proteolysis by GLPS involved primarily the formation of a complex between albumin substrate and GLPS. However, the kinetic analysis showed that a complex formation between substrate and GLPS would not be a sole explanation for the mechanism and more intricate mechanism seemed to be involed in the proteolytic inhibition by GLPS.
There has been recently a rapid and marked advance in Gastroduodenal fiberscopy and endoscopic pancreatocholangiography (EPCG). They have become popular and are now one of the routine valuable examinations. However, observation of the afferent loop and EPCG after Billroth II operation in the stomach is not yet satisfactory at present. The purpose of this study is to develop techniques of EPCG in patients with Billroth II gastroenterostomy. EPCG after Billroth II operation was attempted in 20 cases and of these 15 were successful. A lateral viewing duodenoscopy (JF type B) was applied to 5 cases and was successful in 3. The pancreatic duct was visualized in these 3 cases, and the biliary duct system was in one of them. A forward viewing gastrointestinal fiberscopy (GIF type D, D2, JF type D) was applied to 15 cases and was successful in 12. The pancreatic duct was visualized in 10 cases, the biliary duct system was in 7 cases, both pancreatic and biliary ducts were in 5 cases. It was technically difficult 1) to insert in the afferent loop through the anastomosis 2) to pass through the Treitz's ligament and 3) cannulation from the anal side. The technique of EPCG after Billroth II operation was discussed in this paper. Improvement of the instruments and skillful manipulation of the endoscopy will make it easier to visualize the full length of the afferent loop and to perform EPCG after Billroth II operation.
There were some patients who showed the discrepancy between Indocyanine Green (ICG) and Bromsulphalein (BSP) test. Generally in these patients the BSP retention was higher than ICG. There were few reports about patients who showed high retention of ICG but normal retention of BSP. In this paper two cases with latter type of the discrepancy were reported. Case I-M.N., 50 year old woman (Cholelithiasis), and Case II-K.M., 32 year old man (duodenal ulcer), were admitted. In both cases the laboratory findings were within normal range except for ICG test. The plasma disappearance rate (K) and retention rate (R) of ICG and BSP were respectively as follows-in Case I KICG: 0.023, RICG at 15 minutes: 89%, KBSP: 0.126, RBSP at 45 minutes: 2.9% and in Case II KICG: 0.017, RICG: more than 50%, KBSP: 0.069, RBSP: 4.5%. Three fractional transport rates (a, b, h) were calculated from the plasma disappearance curve following a single intravenous injection of ICG and BSP by an established method. The rates in Case I were aICG: 0.0255, bICG: 0.0158, hICG: 0.0423, aBSP: 0.1331, bBSP: 0.0091 and hBSP: 0.0304. From this result aICG significantly decreased and it was suggested that the impaired plasma disappearance of ICG was possibly the result of low hepatic uptake of the dye. The binding activity of serum protein to ICG in vitro was observed by gel filtration on Sephadex G-200. The protein and ICG were respectively eluted in three main peaks. The protein-ICG binding was apparent in the first peak fraction, whereas less in the second and the third peak fraction in normal control. In these two patients the rate of ICG binding to proteins decreased in the first fraction although the pattern of protein-ICG binding was similar to normal control. The electron-microscopic findings showed the increased reticulum fiber in Disse's space, modification and crystalline-like array of mitochondria, the round cisternae and the small fragments of smooth and rough endoplasmic reticulum and the increase of"lipofuscin-like" lysozome in liver cell. Abnormal retention of ICG was also recognized in father of Case II. From these results the impaired characteristic hepatic removal of ICG in these patients was suspected to be congenital or constitutional.