The continuous and non-invasive monitoring of the hemodynamics as well as of intracellular energy metabolism of the gastric mucosa of rats has been successful by analyzing the reflectance spectra taken by the organ-reflectance spectrum analyzer which was developed in our laboratory. With reduction in blood pressure to a level of 58mmHg by removing blood from femoral artery, the reflectance spectra of the corpus mucosa of the stomach were characterized by 1) decrement of absorbances in the visible region (400-650nm), especially around 577 and 543nm, which indicated a decrease of oxyhemoglobin supply to this region, and 2) appearance of reduced bands of cytochromes in the mitochondrial respiratory chain, which indicated a severe hypoxia in this mucosal region. In contrast, the spectra of the antral mucosa showed only a slight decrement of the absorbances in the visible region with no appreciable change of the spectral pattern. The mucosal hemorrhage and erosions appeared only in the corpus mucosa. These data indicated that acute mucosal hemorrhage and lesions complicating hemorrhagic shock resulted from the disturbances of aerobic energy metabolism of the gastric mucosa following local circulatory insufficiency.
The present study was done in order to investigate the change of pepsin secretion following various operations for gastric and doudenal ulcer. Insulin-and histamine-stimulated pepsin secretion, in comparison with acid secretion, was studied in 140 cases with gastric and doudenal ulcer. Postoperative and follow-up studies were also made in 125 out of 140 cases. Pepsin secretion was expressed in terms of Peak pepsin output (PPO) as well as Peak acid output (PAO). The results obtained are as follows: Pepsin secretion in response to insulin and histamine was different from acid secretion in gastric and duodenal ulcer. In regard to pepsin secretion in response to stimulants, insulin was confirmed to be effectively stronger ability than histamine. Concerning the various types of gastrectomies for gastric ulcer based upon pepsin secretion, pylorus-preseving gastrectomy and segmental gastrectomy are physiological operations, compared iwth Billroth I operation. After vagotomy with pyloroplasty and vagotomy with hemigastrectomy (Billroth I type) the reduction rates in PPO with insulin were 80 and 92% at follow-up, respectively. Similarly, PPO with histamine showed a reduction rate of 52 and 74%, respectively. In the cases performed vagatomy with pyloroplasy when PPO with insulin is less than 100 tyrosine-mg/hr vagotomy may be considered as a"clinically adequate"operation. Concerning the selection of vagotomy with pyloroplasty and vagotomy with hemigastrectomy for duodenal ulcer, the former is suggested for cases with a preoperative PPO less than 500 tyrosine-mg/hr, and the latter should be indicated for those with a value of between 500 and 1250 tyrosine-mg/hr, and the latter should be indicated for those with a value of between 500 and 1250 tyrosine-mg/hr. Further, partial gastrectomy such as Billroth I operation should preferably be empolyed if PPO is in excess of 1250 tyrosine-mg/hr.
This study examined the method of vagal stimulation by insulin hypoglycemia to determine the relation between peripheral vein blood gastrin concentration and gastric aicd secretion. Gastric acid and serum gastrin responses to insulin hypoglycemia with or without medical vagotomy were measured in 49 duodenal ulcer patients. Serum gastrin responses to insulin hypoglycemia rose significantly at 30 minutes, and gastric aicd secretion responded early after insulin injection. Serum gastrin responses to insulin hypoglycemia after medical vagotomy rose similarly at 30 minutes in the cases of insulin hypoglycemia only, but gastric acid secretion were significantly inhibited. These findings indicated that the gastrin release during insulin hypoglycemia is less important in stimulating acid seretion than the direct action of the vagus on the parietal cell, and the release of gastrin by insulin hypoglycemia does not depend soley on the vagus. The greater part of the release of gastrin may depend on the posterior hypothalamo-sympathetic nerve system.
Lymphocyte cytotoxicity was studied by microcytotoxicity assay in patients with chronic liver diseases. Rat liver cell line, established by Coon, was employed as target liver cells. Specific fluorescence of the membranes of these cells was demonstrated by indirect immunofluorescence using rabbit anti insoluble hepatocyte surface membrane antisera. This result indicates that Coon cells retain liver specificity. Peripheral lymphocyte cytotoxicity to the cells was observed in 26 of 28 patients with chronic active hepatitis. This activity was demonstrated in a fraction of non E-RFC but not in E-RFC from the same patients. On the other hand, cytotoxicity to Chang liver cells was found neither in patients with chronic active hepatitis nor in controls, and lymphocytes from chronic active hepatitis did not show cytotoxic to rat foetal cell line. This suggests that lymphocyte cytotoxicity to Coon cells in patients with chronic active hepatitis may be mediated by liver disease specific lymphocyte reaction.
Serum glutamic oxaloacetic transaminase (GOT) isozyme activities were serially measured by an immunological method in 4 cases of hepatic damage following a transient circulatory failure or anoxia episode. When the GOT isozyme activities were plotted on semilogarithmic paper, the activities decreased in a straight line during the first three days after an circulatory disturbance episode. The disappearance rates of GOT isozyme activities were almost same in all cases. The apparent half-life of mitochondrial GOT (GOT-m) was calculated as 0.46 days, while that of cytozolic GOT (GOT-s) was 0.63 days. The disappearance rates of GOT isozymes were analyzed in three acute hepatic disorders with good prognosis, two cases of halothane hepatitis and a case of fulminant hepatitis. When GOT-m activity decreased half in about 0.46 days, the pathogenic factors which were attributed to necrosis of hepatic parenchymal cells were thought disappeared. It was concluded that analysis of GOT isozyme disappearance rates gave usefull informations to evaluate acute hepatic damage.
Hepatic ATP-deficiency induced by ethionine in female rats was restored by intraduodenal administration of ATP in a dose of 2m mol/kg. Administration of ADP was somewhat effective but that of AMP, adenosine and inosine which were well-known as a precursor for ATP-synthesis could not restore hepatic ATP-deficiency in the same dose. Administration of [8-14C] ATP through the duodenum of a male rat resulted in incorporation of larger amount of radioactivity into hepatic ATP-pool than that after administration of [8-14C] AMP or [8-14C] adenosine. Main metabolites of portal plasma after the administration of ATP were determined to be AMP and inosine by means of ionexchange column chromatography but a metabolite, in both cases of the administration of AMP and adenosine, was uric acid only. The results may indicate the utilization of intraduodenally administered ATP for ATP-synthesis not only in the liver damaged by ethionine but also in normal liver.
In order to elucidate the etiologic mechanism of the interaction between the pancreas and parotid gland, male wistar rats of the same litters were used to produce parabiotic pairs. Six pairs which survived the procedure more than 30 days were available for experimentation. In one of each paired rats acute pancreatitis was produced. Amylase concentration in the sera, pancreas and parotid glands in these rats was estimated and histocytological investigation of these organs was made. The following results were obtained: 1. The serum amylase level was elevated in the rats with experimentally induced pancreatitis. It was slightly elevated in the rats without pancreatitis. 2. Organ amylase concentration in the pancreas and parotid gland was reduced in the rats with and without pancreatitis. The reduction of pancreas tissue amylase in the rats without pancreatitis was slight and insignificant. 3. In light microscopy, the pancreas in the rats without pancreatitis was not significantly altered compared to that of the control rats. The parotid gland in the rats without pancreatitis howed apparent atrophic degenerative changes, which were less severe than in the rats with pancreatitis. Electron microscopy revealed that the pancreas in rats without pancreatitis showed similar findings with those of the control rats. In the parotid gland, the findings in the rats without pancreatitis were less severe, but similar to those in the rats with pancreatitis. A humoral transmission mechanism is participating in the development of an interactive response between the pancreas and parotid gland.
Serum ribonuclease (RNase) assay method, using polycytidylic aicd (Poly C) described by Reddi et al was modified, and its diagnostic significance was evaluated on various disease, especially on pancreatic cancer. Serum RNase was demonstrated that its source was pancreas, using Poly C as substrate. It had a pH optimum at 6.5 using 0.1M phosphate borate buffer. Strikingly abnormal elevations occured in the serum RNase of patients with pancreatic cancer. There were no significanct increase in the serum RNase level of patients with chronic pancreatitis. Average RNase values 15 normal persons, 17 patients with chronic pancreatitis, 13 patients with pancreatic cancer, and patients with miscellaneous cancer were 91, 124, 393, 168 units per ml, respectively. In patients with renal insufficiency marked elevation of serum RNase was also observed. On the clinical follow up study decrease of serum RNase levels was seen in patient showing good response to chemotherapy. From these results, serum RNase seems to be quite available diagnostic tool of pancreatic cancer in the presence of normal renal functions.
The patient was aged 71 yrs., female. Tumors respectively of the oral mucosa, lung and stomach in this case were discovered almost simultaneously. The triple tumors were all histologically malignant, while differing from each other in their morphological characteristics. According to statistics based on"Annual of the Pathological Autopsy Cases in Japan", cases of multiple primary malignant tumors in 4 years (1970-1973) amounted to 1, 207 (1.34% of the whole autopsy ases). Of these multiple malignant tumors, double malignant tumors were seen in 1, 157 cases (1.29%), and triple malignant tumors in 49 cases (including our case) (0.05%). Distribution of the sites of the triple malignant tumors shows that the digestive organ was the site of all the 3 tumors in 8.16%, that of 2 tumors in 38.78%, and that of only I tumor in 36.73%. The organs in which triple tumors evelop are also the sites of frequent development of a single tumor.