The clinical significance of serum group I pepsinigen (PGI) level was evaluated by using PGI radioimmunoassay kit. The mean (±SD) level in 69 healthy control subjects was 48.4±17.6ng per ml and the normal rage (mean±2SD) was considered to be from 13 to 84ng per ml. High serum PGI levels were observed in patients with giant rugae gastritis, multiple gastric ulcers, duodenal ulcer and gastric ulcer, and the mean (±SD) levels were 259.5±135.9 (n=6), 296.6±181.9 (n=5), 96.1±38.2 (n=12) and 77.5±33.0(n=35) ng per ml, respectively. Those were singificantly different from the normal level. In addition, rates of high PGI level above the normal range in these diseases were 100, 80, 50 and 45%, respectively. In 3 patients with pernicious anemia and 11 patients with multiple gastric polyps, serum PGI levels were significantly lower than normal value and the mean (SD) levels were 8.1±1.7 and 25.7±17.2ng per ml, respectively. The lower PGI level in both diseases was considered to reflect the gastric mucosal atrophy detected by an endoscopical examination. In addition, among 43 patients with hypergastrinemia (>150pg/ml), all patients with giant rugae gastritis showed high levels of both serum PGI and serum gastrin. This finding indicates that the measurement of serum PGI is useful for the differential diagnosis between hypergastrinemia accompanied with atrophic and giant rugae gastritis.
Rats were immersed in water, and possible changes in the fine structure of the gastric mucosa resulting from immersion stresses, which may appear before the development of macroscopic lesions, were followed up with time under a scanning electron microscope. In an early stage of immersion, the hypersecretion of mucous granules from surface epithelial cells was recognized. It was followed by the flattening of these epithelial cells, then by the enlargement of gastric pits. As the duration of immersion was extended, the epithelial cells became globose and, eventually, they dropped out. And finally surface epithelium disappeared. This disappearance of surface epithelium was considered to represent gastric mucosal lesions observable macroscopically. The changes of the gastric mucosa resulting from water immersion stresses were noticed earlier in the gastric body than in the pylorus. These results suggest that though surface epithelial cells of rat stomach actprotectively against stressor in the early stress stage, subsequent exhaustion of protective potential of the cell by prolongation of the stress period results in mucosal injury.
We divined a rat's neurogenic stress ulcer model. The relative ulcer length (22.33±1.74) of the stress-ulcer model, in which 0.2ml of the arterial blood was injected intracisternally and restraint plus water-immersion for 3 hours was added, approximated the value 21.08±3.34mm which was seen, when restraint plus water-immersion for 9 hours was done in the normal rats. It was markedly higher (p<0.001) than the value 6.63±108mm of the group, in which 0.2ml of saline solution was injected intracisternally and a restraint plus water-immersion for 3 hours was added, indicating an important role played by subarachnoid hemorrhage in production of ulcers in the stress-ulcer-model. Mere intracisternal injection of blood, unaccompained by restraint plus water-immersion, did not produce ulcers. The ulcers occurred in the glandular portion of the stomach and the rumen remained intact. The highest frequency of ulcer occurrence was observed in the corpus excepting the portion of lesser curvature. Histologically, the ulcers did not extend beyond the tunica muscularis mucosae. Using the stress-ulcer-model, several counteracting measures were performed. Ulcer-inhibiting rates were as follows: cimetidine (15mg/kg) 87.5%, (30mg/kg) 85.7%, atropine sulfate (50μg/kg) 70.0%, (8mg/kg) 100%, atropine methylbromide (55μg/kg) 70.0%, combination of cimetidine (15mg/kg) and stropine sulfate (50μg/kg) 49.8%, combination of cimetidine (15mg/kg) and atropine methylbromide (55μg/kg) 34.2%, and truncal vagotomy plus pyloroplasty 97.9% (all significant at p<0.05). Ulcer-inhibiting rates on combination of cimetidine and atropine were significantly low, comparing with that of esch single drug (p<0.02). Ulcer-inhibiting rate at the antrum by administration of cimetidine 15mg/kg was significantly decreased by concomitant administration of atropine, in a small dose (either atropine sulfate 50μg/kg or atropine methylbromide 55μg/kg), and ulcer-inhibiting rate at the antrum by administration of atropine, in a small dose, was also significantly decreased by concomitant administration of cimetidine 15mg/kg (p<0.001). Effect of cimetidine 15mg/kg, or vagotomy in supperssing gastric acidity was significant (p<0.05). Effect of atropine, in a small dose, in suppressing gastric acidity was weak or lacking, and the effect of cimetidine 15mg/kg in supperssing gastice acidity was cancelled by concomitant administration of atropine, in a small dose. The possible mechanism by which the effect of cimetidine was cancelled by concomitant administration of atropine, in a small dose, was discussed.
The precise measurement of plasma secretin by radioimmunoassay (RIA) has been possible. We investigated the importance of gastric acid for the release of secretin during digestion. Then, the relation between gastric pH and plasma secretin level after a meal was studied in patients with duodenal ulcer. After an overnight fast, pH electrode was placed nasally in the distal antrum under fluoroscopic control, and antral pH was recorded continuously before and after a meal. A week later, in all subjects, a second meal test was performed, where cimetidine was administered before a meal. Plasma secretin levels were determined by RIA. Prior to RIA, plasma secretin was purified and concentrated from plasma samples by ethanol extraction according to Chey's method. Antral pH was 3.0±0.7 (SE) in fasting and below 2.0 after a meal. In fasting, mean plasma secretin level was 5.0±0.7 (SE) pg/ml, and increased significantly after a meal (8.9±1.8(SE) pg/ml) (p<0.05). On the other hand, the pre-treatment with cimetidine resulted in a marked rise in antral pH. In these cases, no significant increase in plasma secretin occurred after a meal. It was suggested that the release of secretin depended on gastric acid delivered from the stomach to the duodenum, and that the inhibition of gastric acid by cimetidine showed no significant postprandial increase in plasma secretin.
We studied the enteric nervous system wirhin the tissues of the large intestines of mongrel dogs by applying fluorescent histochemical and histochemical methods. Our results show: 1) Innervation showed various characteristic pictures of distribution depending on region and a notable difference was observed in regards to the myenteric plexus between the proximal large intestine and the rectum. 2) We were able to observe the deep muscular plexus in the ring muscle layer within the tissue of the large intestine. 3) The submucous plexus in the submucous layer arises between two arteries, passes through the mucosal muscular plate and develops branches above the muscular plate and then joins to the mucosal plexus in the mucosa. 4) Using the enzymatic antibody method we were able to identify somatostatin within the mucosa of the large intestine and although it was present in rather minute amounts, we were able to positively confirm its presence.
The aim of this study was to investigate directly, the sugar absroption ability of the small intestine, which had been investigated indirectly by means of the blood concentration and/or the urinary excretion. Forty subjects who had no evidence of small bowel disease were studied. A double lumen tube with balloon was inserted through the anus allowing the end to reach the terminal ileum, under the endoscopic retrograde bowel insertion method, and ileal perfusion using PSP was commenced. 500ml of the test solution containing 25g of D-xylose and 5g of PEG was given orally, and the intestinal contents were aspirated continuously to quantify D-xylose and PEG in the ileum. The absorption of D-xylose and urinary recovery rates at the 5th postcibal hour were 69.2% and 31.4%, indicating that 45% of absorbed D-xylose was excreted in urine. D-xylose absorption rate of the small intestine was directly calculated, and this method can be applied to investigation of absorption of other nutrients as well.
We investigated the effect of prostaglandin F2α (PGF2α) on gastric emptying, small bowel transit time (SBTT), gut hormone release and blood glucose in 8 normal subjects. After an overnight fast, PGF2α at the concentrations of 0.25, 0.50, 0.75μg/kg/min was administered intravenously for 60min. PGF2α caused a dose-dependent acceleration of SBTT with a simultaneous dose-related increase of plasma gut GLI and blood glucose. Negative correlations were observed between the integrated incremental response of gut GLI or that of blood glucose for 120min after PGF2α or saline infusion and SBTT. Gastric emptying, plasma gastrin concentration and plasma motilin concentration did not change significantly during PGF2α infusion. These results raise the possibility that PGF2α causes the acceleration of SBTT directly, not by the increase of motilin release, and that an acceleration of SBTT causes the increase of absorption of glucose and the subsequent increase of blood glucose which may be responsible for the increase of gut GLI.
Twenty patients with unresectable hepatocellular carcinoma were treated by intra-hepatic arterial infusion of MMCmc. Twenty milligrams of encapsulated MMC was infused into the hepatic artery every 4 to 5 weeks. Survival at 3 and 6 months after the initial treatment was 75% and 63%, respectively. The servival rate at 6 months was 83% in 13 cases without tumor thrombosis in the portal trunk or its major branches. Percent regression of tumor ares was evaluated on angiograms, computed tomograms, and ultrasonograms in 16 out of 20 cases 5 weeks after the first treatment. Tumor regression of over 50% was obtained in 38% of the patients, 25 to 50% regression in 19%, and less than 25% regression in 38% of them. In 10 (77%) of 13 cases in which serum AFP level was more than 300ng/ml before treatment, a definite fall in AFP level occurred within one week after treatment. No majior side effects such as bone marrow suppression, hepatotoxicity, and nephrotoxicity were noted.
Twelve cases of so-called limy bile experienced in our hospital were reported here. They consisted of one male and 11 females with a mean age of 49 years. Either the cystic duct or the neck of the gallbladder was obstructed by an impacted stone in 8 cases and a carcinoma of the common bile duct in 1 case. There was no obstruction in the remaining 3 cases in one of which a stone was impacted in the distal part of the common bile duct; limy bile was seen in the common bile duct as well as (in) the gallbladder. The main composition of the limy bile proved to be calcium carbonate and that of the impacted stone cholesterin. On the ultrasonogram the limy bile gave the strong echo with the mild acoustic shadow in the gallbladder. However, it seems difficult to distinguish the limy bile from gallstones by ultrasonography. On the other hand, limy bile, was clearly demonstrated as a high density area in the gallbladder on the computed axial tomogram which, we believe, is more useful for the definite diagnosis of limy bile.
Endocrine function of the pancreas in patients with obstructive jaundice was studied on the basis of plasma glucagon response to intravenous administration of arginine. Immunoreactive glucagon (IRG) levels were determined by radioimmunoassay using the specific antisera, G-8, of Ito. In severely jaundiced patients, whose serum bilirubin levels exceeded 20mg/dl, plasma IRG response to arginine was apparently deteriorated. However, it showed significant recovery after the biliary decompression. When plasma IRG response was correlated with the bilirubin decreasing rate "b", it well maintained within the normal range in patients with the most favorable decreasing rate (the group I; B<-0.09, the peak IRG level=338.9±54.6pg/ml). In the group II, it was significantly deteriorated (-0.09_??_b<-0.05, the peak IRG level=120.2±19.2pg/ml), but recovered markedly after the biliary drainage. In the group III and IV (b_??_-0.05), the peak IRG level never exceeded 200pg/ml and this severe impairment of plasma IRG response persisted long even after the biliary drainage. These results suggest that endocrine function of the pancreas is significantly impaired in patients with obstructive jaundice and the degree of this change correlates well to the bilirubin decreasing rate "b", which seems to reflect the grade of the surgical risk in patients with obstructive jaundice.
Rats were given 200mg/kg body weight of synthetic trypsin inhibitor (TI) by orogastric tube once daily for 10 days. The pancreatic wet weight in rats treated with TI increased by 136%, which was associated with an increase in the amount of protein per DNA, suggesting hypertropy of the pancreas, and with an increase in the total amount of DNA, indicating hyperplasia of the pancreas. Moreover, administration of TI increased the content of enzymes in the pancreas. The dose-response curves for caerulein were similarly shaped in both TI-treated and control rats, but they were shifted 10 fold toward higher concentrations of caerulein after 10 days of TI treatment. Total amount of amylase released from TI-treated rat pancreas was significantly lower than that from the control rat, while the amount of trypsin released from TI-treated rat was significantly higher than that from the control. However, the responsiveness of each enzyme to caerulein was the same when calculated as the percentage of the initial content in the pancreas. Secretory responsiveness of amylase and trypsin in TI-treated rat pancreas was only one fifth of that in control rat pancreas when normalized for the total enzyme content in the pancreas. The present observations have demonstrated that chronic oral administration of TI sufficient to induce pancreatic hypertrophy and hyperplasia in rats increases enzyme content in the pancreas and alters the sensitivity and the responsiveness to caerulein.