Endoscopic control of bleeding esophageal varices by the injection of a sclerosing agent has clinical appeal in view of the high mortality incumbent with general anesthesia and operative intervention. The methodology, complications, and effectiveness of this modality of treatment needs further elucidation. The present study was designed: 1. To develop in dogs an appropriate model for producing esophageal varices. 2. To study the effectiveness of endoscopic sclerosing of such varices. Attempts to produce upper esophageal varices (downhill varices) were made in 35 dogs by partially ligating both the superior vena cava and azygous vein: Five dogs died post-operatively; 22 dogs were examined weekly by fiberoptic endoscopy prior to sacrifice at 12 weeks. Upper esophageal varices were observed in 11 dogs. Four dogs had peroral fiberoptic injection of 5% sodium morrhuate into proven varices prior to sacrifice. Atteempts to create lower esophageal varices were made in 15 dogs by diffuse intra-abdominal systemic portal venous interruption plus creation of a splenic arteriovenous shunt: Eight dogs died post-operatively. Seven survivors were followed by weekly endoscopy prior to variceal injection of 4-8 weeks (3 dogs). Lower esophageal varices were observed in 5 dogs. The varices ranged from 2-8mm in diameter and correlated with the degree of venous interruption. Varices not sclerosed were patent at autopsy; all endoscopically sclerosed varices showed the thrombosis, perivenous fibrosis, and thickening of the intima at autopsy. Three dogs with varices developed superficial ulcers at the site of injection. Histologic studies confirmed gross observations. This study confirms that fiberoptic endoscopic sclerosis of esophageal varices is a safe, reliable, and in experienced hands, a simple technique of thrombosing esophageal varices. The application of this technique to the severely ill patient with bleeding varices is warranted. From the Department of Surgery, Wayne State University, Detroit, Michigan 48201.
In order to investigate the effect of calcium upon gastric secretion, CaCl2 solution was continuously infused intravenously in rats. Saline perfusion performed during calcium infusion at a rate of 4mg/Kg-hr induced the maximal acid output and pepsin output. Calcium infusion also resulted in an increased serum calcium concentration, serum gastrin radioimmunoactivity, and mucosal gastrin radioimmunoactivity of the antrum in contrast to the corpus mucosa which exhibited no increase. However mixed infusion of tetragastrin with calcium did not alter acid or pepsin output, and calcium did not effect gastric secretion in antrectomized rats. It was concluded that antralgastrin played a significant role in gastric secretion associated with calcium.
Plasma gastrin response to test meal (canned liquid food on the market) and gastric emptying of the same meal were examined at the same time in 93 patients with benign gastro-duodenal disease and 30 normal subjects. Gastric analysis was also performed in these subjects. No particular correlation was observed between plasma gastrin response to the meal and gastric emptying except that the significant increase was observed in plasma gastrin response to the meal when gastric emptying was supperssed by anticholinergic. There was also no particular correlation between plasmagastrin response to the meal and the capacity of acid secretion. It was considered that the gastric emptying and the capacity of acid secretion were not so important factor in the plasma gastrin response to the meal. It was concluded that the main factor in the plasma gastrin response to the meal was "functional G cell mass" and that the plasma gastrin response to the meal provided an indirect measurement of the "functional G cell mass".
Histopathological study was made on 401 polyps in the stomach obtained surgically from 257 patients. Polyps were classified intofive groups according to the extent of intestinal metaplasia in the polyp. The incidence of malignant changes increased with the extent of intestinal metaplasia. Of the five groups, the highest incidence (36.1%) of malignant changes was found in the group of polyps composed almost entirely of metaplastic epithelia. Most gastric polyps had tendency to grow pedunclated in shape. But the sessile or subpedunclated shape, regardless of the growing, was preserved in the polyps having two layer structure; the upper layer was occupied by the epithelia of intestinal metaplasia and the lower layer was the epithelia of pseudo-pyloric gland.
The patients with stomal ulcer were studied clinically, paticularly using endoscopy. The endoscopic examinations were applied not only for diagnosis, but also for pathophysiological studies. The gastric mucosal pH, which was directly measured by a micro glass electrode through a fiberscope, showed hyperacidity on residual stomach with stomal ulcer. By endoscopic congo red test, positive results were obtained on the whole residual gastric mucosa except stoma. Observing fine gastric mucosal patterns, by magnifying fibergastroscope (FGS-ML), showed atrophic gastritis was limited is the very narrow area around the stoma of the residual stomach with stomal ulcer. In gastric juice analysis, the patients with stomal ulcer showed increase of total volume, acid output and pepsin output. Serum gastrin levels in the above paticuts were within normal limits in fasting state and after administration of the test meal. As a conclusion, stomal ulcer may be complicated in cases without extended atrophic gastritis of the residual stomach.
The purpose of this investigation is to make clear healing mechanism of round gastric ulcer in comparing X-ray findings with patho-histological findings at each healing stage. In the cases with crossing of convergency of mucosal folds, contraction of gastric wall was mostly noted and regeneration of the tissue was found in small part. On the other hand, in the cases with interuption of convergence of the mucosal folds, the healing was provided mainly by contraction of the gastric wall until that stage and thereafter it was followed by both contraction of gastric wall and regeneration of tissues. The range of healing caused by tissue regeneration was from 4 to 6mm in diameter. The intractable gastric ulcer was therefore considered to be the cases in which contraction of gastric wall does not work and only regeneration of tissue works resulted in prolongation of the healing of ulcer.
In order to presume the prognosis of recurrent duodenal ulcer the stochastic theory of the "Markov's Process" was applied to the 182 recurrent duodenal ulcer patients in whom endoscopic changes of ulcer could be followed. The "transitional probability" in the "Markov's Process" were derived from the results in the first and second years of retrospective study. The expected"transitional probability" obtained by the method of "homogeneous Markov's chain" were fully coincided with the observed values in each year. On the basis of these results, the prognosis of recurrent duodenal ulcers was estimated in the further period. In the period after the sixth year, linear ulcer would be the most presumed figure in the three types of recurrent duodenal ulcers. And fifty percent of all patients with duodenal ulcer would have linear or multiple ulcers in the sixth year. These results were obtained from the presumption that recurrence in recurrent duodenal ulcer patients could contiue in any case.
The present study was done to investigate the influence of biliary diversion upon gastricsecretion in dogs with Heidenhain pouches. Biliary diversion was carried out by the following operative procedures: 1) External biliary drainage; ligation and division of the distal common bile duct and construction of an external biliary fistula by inserting a cannula into the gallbladder, 2)Internal biliary drainage; ligation and division of the distal common bile duct and construction of cholecystojejunostomy en Roux Y by anastomosing the dome of the gallbladder to the jejunum 10cm distal to the ligament of Treitz, with restoration of end-to-side jejunostomy. The following tests in response to a test meal (Dog food 300g) were mainly studied during the control and observation periods after a 3-4 week recovery period; gastric acid secretion and serum gastrin levels. The results obtained are as follows: In external biliary fistula acid secretion from the Heidenhain pouches showed no increase, while in cholecystojejunostomy en Roux Y Heidenhain pouch secretion showed a significant increase in 4 of the 6 dogs, with the increase rate of 110-330%. In both external biliary fistula and cholecystojejunostomy serum gastrin levels showed no significant change. Also, reversion of first cholecystojejunostomy to second cholecystojejunostomy by anastomosing the jejunal loop to the gallbladder caused significant increase in Heidenhain pouch secretion. Acute gastric ulcer developed in 2 of 6 dogs with cholecystojejunostomy en Roux Y. These results indicate that gastric hypersecretion induced by biliary diversion may be related to the possibility of the presence of a gastric secretagogue different from gastrin.
Continuous long-term measurement of intraluminal pH of the alimentary tract in conscious dogs is a valuable means to use in the study of the control mechanism in the digestive system and has therefore been tried, mainly in humans, by means of a glass electrode in situ since 1940, however, there were problems involved in the determination of an electrode site and in keeping an electrode in place for long periods. In the present study, we have developed our own system for measuring pH in situ with a miniature glass electrode inserted through a chronically implanted drainage tube in the alimentary tract. The electrode is a composite type, consisting of a glass membrane (diameter; 2.5mm) and a double glass tube (3×30mm), and a connection to a cable lead was completely waterproofed with silicone. By inserting the electrodes through gastric or duodenal cannulas so that the tips projected 3mm beyond the drainage tube and were in direct contract with the intragastric or intraduodenal contents, the pH of the intraluminal contents could be measured continuously for long periods under stable conditions. In an attempt to make a quantitative analysis of pH changes, a pH meter was connected to integrators to integrate pH changes above and below 7.0 separately as a product of time and mV. Although such quantitative analysis has not yet been theoretically elucidated, it is useful in determining what changes have occurred over an extended period. Information obtained by this method will provide us with a key to the releasing mechanism of gastrointestinal hormones and the pathogenesis of duodenal ulcer.
The occurence of the disseminated intravascular coagulation (DIC) in patients with fulminant hepatitis has been recently reported. In this study, abnormalities of coagulation and fibrinolysis in 30 rabbits with experimental CCL4-induced acute hepatic failure were investigated. The prothrombin time and partial thromboplastin time showed to be remarkably prolonged 24hrs after oral administration of CCL4. Levels of fibrinogen and platelet count were decreased, and fibrin/fibrinogen degradation products was increased at the same time. In addition, one rabbit revealed disseminated fibrin thrombi in autopsy. In 9 rabbits in which heparin was given by continuous infusion pump for 48hrs just after the administration of CCL4, the fibrinogen level was improved remarkably and prothrombin time, partial thromboplastin time and factor VIII level were also slightly improved. These findings suggested that, in addition to diminished svnthesis, of coagulation factors, DIC was involved in CCL4-induced acute hepatic failure and contributed to the haemostatic disorder.The treatment with heparin seemed to be effective in this series.
Human serum ligandin was quantitated by means of double antibody radioimmunoassay method and its clinical implication of serum ligandin in patients with liver disease was evaluated. Standard curve showed satisfactory linesrity from 5ng/ml to 1000ng/ml. The normal value was 10.2±3.5ng/ml, and higher values were obtained in the acute phase of various liver disease. Serum ligandin levels and serum transamirase activities were correlated in acute hepatitis. Serum ligandin levels were decreased more rapidly than serum transamirase activities on its clinical improvement of acute hepatitis. These findings, therefore, indicated that ligandinemia might be due to the release of ligandin from the damaged liver cells.
Hepatic vein catheterization was performed in 70 patients with liver diseases, and the radiographic findings of hepatic vein branches and sinusoidal fillings were classified into I-IV and a-c groups, respectively, in the order of seventies of changes. The usefulness of this procedure was assessed by comparing the venograms with other tests and measurements. 1) Of the 41 patients with liver cirrhosis, 73.2% belonged to Grade IIIor IV. In contrast, 79.3% of the patients with other liver diseases showed changes of Grade II or a milder degree. 2) When compared with the laparoscopic findings, 86.4% of the patients with 'a' group findings had a smooth liver surface and all of the 'c' group had nodules of 3mm or larger. 3) These of radiographic changes of hepatic veins and sinusoidal fillings were well reflected in the grade of esophagial varices. It was concluded that if 2 or more of the following three changes were present, i.e. changes of III-b or severer in the Venogram, 150mmH2O or higher in the corrected WHVP, and 45% or less in the ICG extraction rate, a diagnosis of liver cirrhosis may be made with a 80% probability. In the mean time, if none of these changes were present, cirrhosis may be excluded with a similar probability.
Relationship between pancreatic and bile duct was analysed in eleven cases with congenital biliacy dilatation diagnosed by ERCP, especially in regard to the types in confluenting bile duct with pancreatic duct and the forms of their terminal portion. Generally, the author could classify 5 categories (Type I-Type V) in the type of their confluence.Abnormality in the type of confluence was disclosed (Type IV or Type V) in eight cases (73%). Both type were characterized by two findings. One was the stricture of the terminal portion of bile duct, at the point just over the junction with pancreatic duct. And another was the prolongation of the common channel. Depending upon the type of their confluence, following abnormal features were disclosed. In Type IV in which bile duct joined into pancreatic duct, a defect of the notch at the opening of pancreatic duct was found. In Type V in which bile duct joined into pancreatic duct, a dilatation of pancreatic duct in its head portion was seen. Our results suggest that both congenital and acquired factors are concerned with the pathogenetic mechanism of congenital biliary dilatation. That is, the type of abnomality in confluenting bile duct with pancreatic duct and the reflux of pancreatic juice into bile duct would contribute to developing biliary dilatation in the disease.
Three cases of chronic intrahepatic cholestasis with Sjögren's syndromes were reported. Sjögren's syndrome was diagnosed by clinical features, Schirmer test and sialography in case 1 and 2. In case 3, the syndrome was suspected by clinical pictures and positive Schirmer test. All cases were female of over middle age, and serum alkaline phosphatase was makedly increased. Although increased IgM and positive anti-mitochondrial antibody suggested primary biliary cirrhosis in case 1 and 2, degenerative and necrotic alteration of the bile ducts which was pathognomonic to primary biliary cirrhosis was not observed. In case 3, lymphocyte and plasma cell infiltration and decrease and destruction of bile ducts were evident histologically. Sjögren's syndrome is suggested to be a generalized disease with hypofunction of exocrine glands by autoimmune mechanism. In some cases of intrahepatic cholestasis including primary biliary cirrhosis, autoimmune reaction is suspected by the positive autoantibody. Interrelation of Sjögren's syndrome and intrahepatic cholestasis was discussed.