The CEA levels in basal gastric juice were determined by CEA RIA kit (Dainabot). The levels in groups with atrophic gastritis and gastric carcinoma of its early and advanced stages were significantly higher compared with those in normal control group (p <0.01) . Since the upper limit of normal CEA level in basal gastric juice was estimated up to 3.0 ng/ml, CEA positivities for evaluation of diagnosis of gastric carcinoma on its early and advanced cases were 80 and 70%, respectively. However, false positive cases in peptic ulcer and atrophic gastritis were found 20% and 86%, respectively. The CEA levels showed a good correlation with the presence of atrophic gastritis accompanied with intestinal metaplasia and the acidity of the basal gastric juice. Therefore, CEA levels were found to be significantly lowered in acidic condition of gastric juice after tetragastrin stimulation compared with the higher prestimulation values, and the CEA activity determined by RIA was markedly decreased when standard CEA was incubated in gastric juice of pH 1.9 at 37°. These facts revealed that CEA or CEA-like substance was easy to break in acidic gastric juice, presumably digested by pepsin. In addition, since NCA was often detected in 5% saline solution of the lyophilized gastric juice by Ouchterlony's method, it was suspected that determination of CEA RIA system should be affected by the increase of NCA in gastric juice.
The effect of intensive antacid (aluminum hydroxide, 24-48g. 12-24 times per day) or cimetidine therapy (1200mg. 4 times per day) was investigated in 30 patients with massive upper G-I bleeding from acute gastroduodenal lesions. The bleeding stopped in only 10(27.8%) of 36 patients in control group but in 14(73.7%) of 19 patients in intensive antacid and 8(72.7%) of 11 patients in cimetidine group, respectively. The bleeding from hemorrhagic gastritis was controlled successfully in all patients by the latter two treatment. However, the bleeding from acute ulcers with ruptured vessels on the crater was unable to control. Large amounts of aluminum hydroxide induced hypophosphatemia, hypophosphaturia, hypercalciuria and a slight increase of serum aluminum. Adverse effect of cimetidine was not observed. The results indicate that intensive antacid or cimetidine is of value in the management of massive G-I bleeding from acute gastroduodenal lesions.
Measurements of continuous changes in intraduodenal pH were carried out by means of a miniature pH electrode inserted into the duodenum through a chronically implanted duodenal cannula in conscious dogs. Gastric motor activity was measured by strain gage force transducers chronically implanted onto the serosal surface of the stomach. It was found that there exist diurnal changes in intraduodenal pH consisting of the three periods; the weak acid period (pH 7.0-4.0), storng acid period (pH 8.3-1.0) and alkaline period (pH 8.3-7.0). These three periods corresponded to those of the three different gastric motor patterns, the digestive, intermediate and interdigestive state. Furthermore, it was indicated that the strong acid period is most adequate for endogenous release of secretin and the alkaline period for motilin release. These findings suggest that control of gut function is closely related to intraduodenal pH changes through endogenous release of gut hormones.
The purpose of this study is to assess the re of microtubules in the process of absorption and transportation of long chain fatty acids into intestinal lymph and to clarify whether intestinal alkaline phosphatase (IAP) plays a part in the phase of lipoprotein release to lymphatics during fat absorption. Male Wistar rats provided with intestinal lymph fistula were used for the absorption studies. Mixed micellar solutions of fatty acids were administered into the duodenum of rats. Effect of colchicine, an inhibitor of microtubular function, on the fatty acid absorption and alkaline phosphatase activity during fat absorption were studied in intestinal lymph. In colchicine-treated rats, the lymphatic absorption of intraduodenally administered long chain fatty acids was decreased, however, there was no significant difference of colchicine inhibition between the lymphatic absorption of palmitic acid (saturated) and linoleic acid (unsaturated). Administered fatty acid was transported slowly to lymphatics almost in form of free fatty acid when colchicine was treated. Microtubular system was revealed to be necessary for the lipoprotein release from intestinal epithelial cells to lymphatics during fatty acid absorption. In control rats, the increased activity of TAP in intestinal lymph was observed in parallel with the amount of absorbed fat. However, in colchicine-treated rats, the equal amount of output of TAP to lymphatics was also observed in spite of the decrease of linoleic acid absorption. These results suggest that microtubular system does not take part in the transportation of TAP into lymphatics and TAP may not play a possible role in the phase of secretion of lipoprotein from intestinal epithelial cells during the absorption of long chain fatty acid.
K-cell population in peripheral lymphocyte fractions from patients with drug-induced allergic hepatitis were analysed with a microscale method using ADCC reaction. The level of cells active in ADCC reaction were shown to be significantly higher in the patients than those of normal individuals. Although the level of K-cell population were lowered by impairing the monocyte function with silica treatment, the addition of supernatant of macrophage culture caused an appearently increase of K-cell population. By a gel filtration, a active substance which caused the increase of K-cell were fractionated from supernatant of macrophage culture.
Osmotic resistance using CPC method, erythrocyte lipids and plasma lipoproteins in patients with hepatobiliary diseases were studied. In cholestasis with high concentration of plasma Lp-X, the osmotic resistance was increased intensively and marked elevation of both cholesterol and phospholipids in their erythrocyte were observed. On the other hand, in other hepatobiliary diseases, only cholesterol was increased in their erythrocyte in spite of the increased osmotic resistance. When cholestasis was removed by PTC drainage, the decrease of cholesterol and phospholipids in equal molar ratio was observed with the normalization of osmotic resistance. Lecithin was the primary phospholipid of increased phospholipids in erythrocyte with cholestasis, and it's fatty acid composition of acyl chain resembled with that of Lp-X. In conclusion, there are two kinds of mechanism that increase osmotic resistance in hepatobiliary diseases, one is the high cholesterol content of erythrocyte with decreased LCAT reaction, and the other is the high cholesterol and lecithin content of erythrocyte due to the fusion of Lp-X. The measurement of osmotic resistance facilitates the clinical evaluation of the degree of cholestasis and the evaluation of the treatment in cholestasis i.e. PTC drainage.
Among 20 cases with idiopathic portal hypertension, 17 cases revealed abnormal findings in the intrahepatic bile ducts by serial section observations. Five cases showed wide-spread distribution of damaged bile duct (epithelial degeneration or proliferation), and 3 of them also revealed segmental distribution of marked periductal inflammation. Four cases showed focal distribution of damaged bile ducts (degeneration or proliferation). And proliferation of ductules or small interlobular bile ducts was seen in 8 cases. Wide-spread bile duct damages seen in 5 cases were thought to be intimately associated with the development of portal hypertension.
Intravenous glucose tolerance test was performed in sixteen cases with obstructive jaundice and in thirteen normal persons as control. Jaundice group showed higher fasting blood sugar level, and after glucose injection there were glucose intolerance and poor insulin reponse of the early phase. In this group, serum potassium level decreased after glucose injection and did not return to the fasting level even 120 minutes after. Serum inorganic phosphorus level decreased after glucose injection in both groups, but that of jaundice group was higher during the observation, with low reduction rate. Fasting blood cortisol and cathecolamines level were higher but decreased much more after glucose injection than those in control group. In is concluded that glucose intolerance in obstructive jaundice is closely related to the accelerated glycogienolysis or gluconeogeness based on poor insulin response, lowed serum potassium, elevated serum inorganic phosphorus and abnormal adrenal function.
The DNase I and DNase I inhibitor in duodenal juice obtained after administration of Pancreozymin and Secretin were assayed in patients with various pancreatic diseases. The DNase I output was much lower in patients with chronic pancreatitis than control subjects. The decrease of DNase I output was observed even in patients with chronic pancreatitis suspected, who indicated rather obscure distinction from the control subjects, as judged by the ordinary methods of PS test. In addition the DNase I inhibitor output was much lower in patients with chronic pancreatitis, but in patients with chronic pancreatitis suspected the increase of DNase I inhibitor output was observed. It was thought that the decrease of DNase I output in patients with chronic pancreatitis suspected was due to the increase of inhibitor output. These results imply that the DNase I output might indicate the exocrine function of pancreas precisely, and make the early detection of pancreatic diseases possible.