The elucidation of the pathophysiology of peptic ulcer during recent years has resulted in a decrease in the incidence of postoperative peptic ulcer, but it has not yet been totally eliminated.
For the purpose of preventing postoperative peptic ulcer, the authors perfurmed a pathyphysiological study of the condition from the standpoint of endo-exocrine functions by classifying the cases into three groups: Group I: Those who has received total resection of the pyloric gland, Group II: Those in whom the pyloric gland was retained, Group III: Those in whom the pyloric antrum was retained following the Billroth II operation. The findings were as followl: (1) In patients who underwent operation for duodenal ulcer and whose postoperative MAO value was greater than 1OmEq, the risk for recurrence was great. (2) In Group III, the B. G (basal gastrin level) and I-IGR (integrated gastrin response to insulin hypoglycemia stimulation) were both significantly higher than those in the other two groups, but the IGR was inhibited by the administration of secretin. (3) Group II revealed slightly greater response to T-IGR (meat extract stimulation) and C-IGR (calcium stimulation) than Group I, but the differences were not statistically significant.

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The property of prostaglandins (PGs) protecting the gastrointestinal mucosa against various ulcerogens was called cytoprotection by Robert, and has been given marked attention. However, concerning endogenous PGs in the gastric mucosa, only a few reports were present. Recently, the authors established the method of the intramucosal PGE₂ determination. Effects of indomethacin and mefenamic acid to PGE₂ levels in the gastric mucosa were investigated in this paper.
PGE₂ levels in the antral mucosa were significantly high (3.95±0.55 tg/g w.w.) compared with the levels in the fundic mucosa (1.76±0.13). PG₂ contents of both the fundic and the antral mucosa were markedly reduced on thirty minutes after the oral administration of indomethacin at a dose of 6 mg/kg (0.41±0.15 and 0.72±0.33, respectively). On the other hand, no significant change was detected after mefenamic acid administration (200 mg/kg per os). Intramucosal cyclic AMP contents were significantly reduced in the indomethacin group.
In these results, it is suggested that differences between the fundic and the antral levels of intramucosal PG₂ may be correlated with location of the mucosal damage. It is also suggested that the degree of intramucosal PG₂ inhibition may be different between the two non-steroidal antiinflammatory compounds. Further, it is more likely that intramucosal PGs may act through cyclic AMP system.

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For comparative patho-historogical purposes, studies were made on the vascular system supplying infiltrative and proliferative tissues of gastric cancer, and on the vascular system by which chemotherapeutic drugs reached gastric cancer tissue. Plastic models were made of the vasculature of resected human gastric cancer and gastric cancer produced experimentally in rats. These plastic models were examined by scanning electronmicroscopy.
The vessels in tumors were found to be fine networks of high vascular density. The vascular density was similar in gastric cancers of different histological types (structual atypism), but it was higher in medullary carcinoma than in scirrhous carcinoma. A classification of the vascular pattern into three types with respect to tumor progression was so similar to INF classification that the patterns of infiltration and proliferation in peripheral portions could be recognized on the basis of the vascular structure. The vasculature of benign gastric ulcers convergend linearly from the periphery to the focal site, and thus its appearance differed from that of cancer. The vascular structure of gastric cancer in rats was found to be similar to that of human gastric cancer.

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CEA measurements have been made in randomly selected 644 patients with gastrointestinal malignancies and in 384 patients with gastrointestinal benign diseases. CEA measurement was unlikely to be of value as a screening test for the detection of malignacy, however, elevation of serum CEA levels more than 5 ng/ml in CEA RIA KITT suggested the necessity of cancer survey in the patients. In postoperative patients of colorectal cancer, serial CEA measurements seemed to have beneficial effect in early detection of liver metastasis, while local recurrence did not reflect serum CEA elevation.
Elevated CEA levels occurred in a relatively high proportion of patients with liver dysfunction but there did not appear to be any real relationship between serum CEA levels and liver function tests.
CEA levels in effusion fluid correlated well with the presence of carcinomatous serosistis.

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Breath hydrogen measurement by our apparatus with a closed system was performed in 18 healthy subjects and a patient with malabsoption syndrome after administration of 5, 15, and 25g of D-xylose. By the same method, breath hydrogen excretion was determined after administration of 13g of lactulose and 50g of glucose, respectively. The more D-xylose was administered, the more breath hydrogen was excreted. In a group where a 25g of D-xylose was administered, the maximum amount of expired breath hydrogen was less than 0.28ml/min..
In the D-xylose administered group including a patient with malabsorption syndrome, there was a good correlation between the max. Amount of breath hydrogen and a 5 hour urinary excreted D-xylose. Since a good correlation was observed in the group where a 25g of D-xylose was given, a 25g of D-xylose may be considered as the optimal dose for the breath hydrogen test.
In summary, the breath hydrogen measurement by administering 25g of D-xylose might be said a useful clinical tool in the diagnosis of malabsorption syndrome.

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When lymph node lymphocytes from the tuberculi-sensitized guinea pigs were stimulated in vitro with PPD and the culture fluid was injected into the mesenteric vein of rats, a marked reduction in bile flow was observed. The culture supernatant contained the cholestatic activity was fractionated into six fractions by a gel filtration using Sephadex G-75 column. Both cholestatic activity and the macrophage migration inhibitory factor (MIF) activity were found predominantly in fraction No.4. The active fraction (No.4) was further fractionated into five fractions by a DEAE-cellulose column chromatography and found that the cholestatic activity was detectable in two fractions (fraction No. 1 and No.5), which MIF activity was detected in fraction No.1 and No.5.
These results suggest that the cholestatic factor may be different at least partially from the MIF.

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In order to study the glucose intolerance in alcoholic liver injury, the blood sugar and serum insulin (IRI) were determined during 50 g-oral glucose tolerance test (GTT) in 88 patients of alcoholic liver injury (alcoholic group) and 96 patients of nonalcoholic liver disease (non-alcoholic group). GTT was performed over one month after abstinence in all cases of alcohol group. In 25 patients of them, GTT was studied not only over one month after abstinence but also within one week after abstinence. Pancreozymin-secretin test was also performed in 65 patients of alcoholic group and 40 patients in non-alcoholic group.
Within one week after abstinence, alcoholic group showed glucose intolerance more frequently than non-alcoholic group. After the abstinent period over one month, glucose intolerance was so remarkably improved in many cases of alcoholic group that there was not significant difference in blood sugar level during GTT between alcoholic group and nonalcoholic group. The level of 30'ΔIRI/ΔBS increased following abstinence comforming to the improvement of glucose intloerance or serum transaminase levels. However, except cirrhotic cases, the frequency of overt diabetic state was more common and the insulin secretory response was lower in alcoholic group than in nonalcoholic group. Moderate to severe pancreatic exocreine insufficiency was more frequently (16.1%) in non-cirrhotic alcoholic group than in non-cirrhotic non-alcoholic group and most of cases showing overt diabetes had moderate to severe pancreatic exocrine insufficiency in non-cirrhotic alcoholic group.
From these results and our previous investigation, it is concluded that pancreatic disorder is important factor contributory to the glucose intolerance in non-cirrhotic alcoholic group. In cirrhotic alcoholic group, pancreatic exocreine function was almost normal and, therefore, we could not find the influence of pancreatic disorder on glucose tolerance.

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To compare the efficacy of the methods to measure the insulin secretory capability, 15 patients with liver disease were studied with intravenous infusion of 0.5g glucose/kg ideal body wt. over 2min or with oral intake of 50g glucose. Portal and peripheral blood insulin and C-peptide levels were measured simultaneously for 2 hours after glucose infusion, and ΔIRI/ΔBS was measured using peripheral blood insulin and glucose levels before and at 30min after glucose intake.
With glucose stimulation, portal vein levels of insulin and C-peptide showed a peak at 2min and again around 60min, and the molar ratios of C-peptide to insulin in portal blood fell rapidly and thereafter kept a constant value relatively.
Insulin secreted (area under curve or AUC 0-60min for portal blood IRI) showed a significant correlation with AUC 0-60min for peripheral blood IRI (γ=0.60, p<0.02), with JIRI/4BS (γ=0.65, p<0.01), but not with AUC 0-60min for peripheral blood CPR. Values for glucose disappearance rate (K_G) showed a siginificant correlation with insulin consumed (AUC 0-60 min for portal blood IRI minus AUC 0-60min for peripheral blood IRI) (γ=0.79, p<0.001).
These results suggest that the combination of KG value and AUC 0-60min for peripheral blood IRI may be a better method to predict the insulin secretory capability in patients with liver disease than the others.

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The effect of long term administration of synthetic trypsin inhibitor on exocrine pancreas was investigated in in vitro perfused rat rancreas. The rate of flow of pancreatic juice and the rate of output of amylase were similtaneously determined in the isolated perfused pancreas from male Wistar rats which were treated a 20-day course with either synthetic trypsin inhibitor (200mg/kg) or 0.15 M NaCI solution. In trypsin inhibitor treated rats, the wet weight of pancreas and the amylase content of the pancreas were increased about two fold of those in control rats. The basal rate of flow and the maximal rate of flow of pancreatic juice in response to 0.1 ngf ml caerulein in trypsin inhibitor treated rats were significantly higher than those in controls. On the other hand, concentration of amylase in pancreatic juice and the total output of amylase in response to direct stimulation with caerulein were significantly impaired in the trypsin treated group. From the present observation, it could be said that the enzyme secretion pattern of the hypertrophied pancreases of rats treated with trypsin inhibitor is different from normal.

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