1984年 · 第04卷第01期

Four hundred and forty-eight cases of chronic gastritis, chiefly chronic atrophic gastritis, were collected and dynamic changes in the intestinal metaplasia (IM) (530 sites) , dysplasia (146 sites) and the atrophy of gastric glands were studied during a period of 2-10 yr. The severity of glandular atrophy and IM advanced usually with the prolonged duration of observation. On the contrary, the possibility of reversal of dysplasia was independent of the length of observation period. Nine cases of gastric cancer were diagnosed during observation, 5 of them were discovered between 3-6 yr, and the others were within 3 yr. Three out of 315 patients with only IM developed carcinoma, while 6 out of 112 patients with both IM and dysplasia developed cancer. This study shows that dysplasia and IM especially in moderate and severe degree have much to do with gastric carcinoma.

Five hundred thirty-three cases of chronic atrophic gastritis (GAG) diagnosed by gastroscopy and biopsy were collected from 5 medical units. Parietal cell antibody (PCA) was examined in all cases. Eighty-seven cases were PGA positive (16.3%) , the other 446 cases were PCA negative (83.6%) , Gastric carcinoma was detected in 8cases during the follow-up period of 1-6 yr. Five of them were PCA positive and 3 were PGA negative. CAG was classified into 2 types, A and B, by Strickland according to his result of PCA exam. Type A is of PGA (+) , and type B is of PCA (-) . Gastric carcinoma was found only in the group of type B. Our data are quite different from the experience of Strickland. Therefore, in our country, it seems that there is little significance to classify CAG into type A and B based on either the result of PCA exam or the location of CAG lesion, because gastric carc inoma was not limited to PCA (—) patient.

The relationship between G-cell density in antral biopsies, gastric acid secretion and serum gastrin levels in 48 patients with duodenal ulcer was studied. No difference of G-cell density was found in all age and sex groups. There was positive correlation between G-cell density and serum gastrin level after fat-protein meals, but not so between fasting serum gastrin levels and G-cell density, basal acid output and G-cell density, and peak acid output and G-cell density.

Endoscopy was performed in 30 healthy elderly. Among them 17 were males and 13 females, ages ranged 60-88, mean 74.6. The histopathology of the gastric mucosa taken at the time of endoscopy revealed one elderly was consistent with superficial gastritis, 4 had degenerative lesions in both the antrum and the body, and the remaining 25showed mild or moderate degree of atrophic gastritis associated with degenerative changes to some extent. It is concluded that the mild form of atrophic gastritis is common in the healthy elderly, and degeneration is probably the most important pathogenetic factor.

Many studies have suggested that prostaglandins (PGS) , especially the E type, are cytoprotective to gastric mucosa exposed to a variety of necrotizing agents and nonsteroidal antiinflammatory agents, such as aspirin or indomethacin, which have been shown to cause irritation, ulceration and bleeding of the gastric mucosa. The results of our clinical and experimental studies in determing the levels of PGE in the gastric mucosa indicate that (1) the gastric mucosa of rat and human subject produces much more PGE in the antrum than in the fundus; (2) nonsteroidal antiimflammatory agents such as aspirin may lead to the reduction of PGS biosynthesis, as a result of promotion of the gastric mucosal injury; (3) 1% or less of the antisecretory dose of PGE (including endogenous cytoprotection PGE induced by 20%ethanol) can protect gastric mucosa, indicating that a way of preventing ulcer caused by drugs clinically has been found; (4) increase in PGE contents in the gastric mucosa has been observed in patients with chronic atrophic gastritis and superficial gastritis, which differ significantly from the findings in healthy subject. The possibility of PGE involvement in the pathogenesis of atrophic gastritis should be considered and verified through further studies.

The purpose of this investigation was to observe the effect of intiacerebroventricular (IGV) injection of humic acid on the gastric acid secretion in rat. Noble's method was used for ICV injection, and the doses were 0.12, 0.16, 0.20 and 0.25 mg/kg. Gastric secretion 4 hr after pyloric ligation according to Shay's method was measured. The results showed that IGV injection of humic acid significantly reduced gastric secretion, the response was dose dependent.

Estimation of serum immunoglobulin levels and immunoregulatory activity of peripheral blood lymphocytes had been performed in patients with liver cirrhosis, chronic active hepatitis and normal persons. Immunoregulatory activity was expressed as suppressor cell activity, which was measured by the relative lymphoproliferative response to Con-A. The patients with chronic liver diseases had lower suppressor indices (1.32±0.73) as compared with normal controls (2.43±0.46) . Most of the patients with chronic liver diseases had elevated serum immunoglobulin levels, and a negative correlation between suppressor index and serum globulin p<0.01), particularly serum IgG p<0.0l) existed. The results suggest that suppressor cells might, in vivo, modulate immunoglobulin production.

The effect of liver reticular endothelial system (RES) on galactosamine (GalN) -induced fulminant hepatic failure (FHF) rats was evaluated by means of RES block with the use of mesenteric injection of Indian ink. Thirty-seven Wistar rats were used. The results revealed that the liver damage in the ink blocking FHF group was severely exaggerated, SGPT was increased more than in the FHF control group (p<0.001) . Serum bilirubin was also augmented. No obvious liver damage was found in the ink injection control group. The survival rate of the ink blocking FHF group was only 31.3%, while that of of the FHF control was 81.3% (p<0.002) and no death was found in the ink control group. Injection of galactosamine after laparotomy or cannulation of femoral vessels had a lower degree of liver damage and mortality than injection before surgery. The possible relationship between FHF and RES function is discussed. It is presumed that RES function disturbance is a very important factor in the formation of acute liver damage. This study may be of some value in the therapeutic research of FHF.

Aramine, phentolamine, ipilocarpine and scopola- mine were administered into the portal vein of 30 anesthetized mongrel dogs, and their effect on the hepatic venous pressure, portal venous pressure and hepatic arterial blood flow were observed. The results showed an elevation of portal venous pressure, reduction in protal venous flow and increase in portal vascular resistance following aramine administration. These effect could be blocked by phentolamine, indicating the existence of α-adrenergic receptors in portal vascular beds. Phentolamine reduced the vascular resistance of the liver, and pituitrin constricted the arteriols of spleen, stomach and intestine, the administraetion of each of the drugs resulted in lowering of portal venous pressure. Pilocarpine produced portal vascular respons similar to that of aramine, however in a lesser degree, which could not be blocked by scopolamine. Therefore, the presence of cholinergic receptors in portal vascular beds remains uncertain.

With the help of Type 835- 50 hyperspeed analyser, quantitative analysis of amino acids in the cerebrospinal fluid(CSF) of 4 patients with hepatoencephalopathia was carried out. Ten patients with nonhepatic disease and normal CSF served as control. In the CSF of patients with hepatoencepaalophthia, the contents of methionine were 15 times, phenylalanine tyrosine 7 times, histidine, glycine, alanine and lysine were each 2-3 times higher than that of the control group. There was no difference in the amount of valine, leucine and arginine, while the amount of isovaline was only half that of the control group. The value of CSF BCAA/AAA was markedly decreased in the hepatoencephalopathia group. There was no significant difference in the amount of CSF amino acids between acute and chronic hepatoencephalophathia. However, in chronic hepatoencephalopathia, the CSF ammonia content was 2 times higher that that of the acute cases. This implies that there might be a closer relation between ammonia poisoning and chronic encephalopathia.