1984年 · 第04卷第04期

Serum pancreatic polypeptide (PP) determined by radioimmunoassay is described in detail. The assay was found sensitive and specific in detecting 25 pg/ml of PP in serum. The basal levels of PP in 112 normal adults at 20-78 years old were 32-380 pg/ml. The serum level was found correlated significantly with age. The upper levels of normal basal serum PP in the groups of 20-29, 30-39, 40-49 and ≥ 60 years old were 151, 162, 215, 345 and 417 pg/ml (mean ±2 SD) respectively. In addition, PP levels were determined after ingestion of 2 boiled eggs in 20 healthy persons. The mean concentration eleven-fold increased the basal level within 30-60 min after taking the 2 eggs.

Gastrin in gastric juice was determined by radioimmuno-assay in 25 patients with chronic gastritis and 20 with peptic nlcer. Except the patients with atrophic gastritis in corpus, the amount of basal gastrin released in gastric juice was not significantly different in patients with superficial gastritis, atrophic gastritis in antrum, gastric ulcer and duodenal ulcer. Instillation of a 10% peptone solution (pH 5.5) induced a significant and simultaneous increase of acid secretion, and amount of gastrin released into gastric lumen, together with elevated serum gastrin level. The peaks of gastrin in gastric juice were similar in all groups of patients (P>0.05) . There was a close relationship between the levels of gastrin in gastric juice and in serum.

After iv injection of 1,000,000 to 1,500,000 CPM of lebelled gastrin-17 in 5 rats, no radioactivity was detected in gastric juice in 1 hr, suggesting that gastrin in gastric juice is not coming from the serum. Thus, we believe that gastrin released from antral G cells goes into blood circulation as well as into gastric lumen directly.

This paper presents the study on the acid secretory function with graded pentagastrin dosage test in the 55 cases of duodenal ulcer and 31 cases of normal control. Pentagastrin was given intramuscularly with the dosage of 1 μg/kg, 1.5μg/kg, 2 μg/kg and 6 μg/kg. The interval between each graded dosage was 30 min. The results revealed that using the standard dosage of pentagastrin (6 μg/kg) , BAO=10.73± 9.23 mmol/hr and PAO = 43.05± 14.03 mmol/hr in the duodenal ulcer group, while BAO = 4.25 ± 5.48 mmol/hr and PAO = 26.87 ± 12.8 mmol/hr in the control group. When the dosage of pentagastrin≤ 2 μg/kg was used, PAO appeared in the 39 cases (71%) of the duodenal ulcer group and 12 cases (39%) of the control group. In all the other cases, PAO appeared in the dosage of 6 μg/kg of pentagastrin. The study suggests that both the increase of parietal cell mass and of the reactivity of the parietal cell to acid stimulant are the important factors in the pathogenesis of duodenal ulcer.

Total and free plasma tryptophan and other biochemical parameters were tested in 20 normal individuals as well as 52 patients with liver diseases, including 20 patients with hepatic coma. In addition, 12 pigs with induced acute is-chaemic hepatic failure were also experimentally studied. The results revealed that the plasma tryptophan levels were closely correlated with the presence, grade and evolution of hepatic coma. In hepatic coma the free plasma free tryptophan level was more significantly elevated than total tryptophan level. The molar ratios of plasma free tryptophan to BCAA, BCAA + AAA + Met and total tryptophan were correlated with the presence of hepatic coma. Furthermore, the clinical investigation showed that plasma free tryptophan and total tryptophan correlated significantly with serum total bilirubin and prothrombin time respectively. The ratio of free tryptophan /total tryptophan also correlated significantly with prothrombin time. The authors point out that the value of plasma tryptophan (mainly free tryptophan) might reflect the parenchymal function of liver and the prognosis of the disease.

Determination of serum autoantibody against gastrin-producing cells (GCA) by immunopexidate staining technique is described in detail. The serum of 375 individuals was tested for GCA and autoantibody against parietal cells (PCA) . In 39 cases of histologically proved chronic atrophic gastritis (CAG) localized on gastric antrum (CAAG) , GCA was found in 10, PCA in 2. In 16 localized on gastric body (CAAB) , PCA was found in 3 and no GCA in any. In 51 cases involving both the antrum and body, GCA was found in 3, PCA in 9. These findings demonstrated that autoimmuno-reaction played a significant role in the genetics of CAAG and CAAB. Therefore, GAG might be subdivided into 4types (A₁, A₂, B₁, B₂) according to its location and the presence or absence of autoantibody. In superficial gastritis (SG) the distribution of autoantibodies was essentially similar to that of CAG, suggesting their common immunological origin in some cases. Furthermore, this study also showed that there was no correlation between the age of the patients and the presence of autoantibody in CAG.

The test of serum gastrin response to protein-rich meal in 35 patients with chronic atrophic gastritis and 11 normal individuals as control, and the measurement of their antral gastrin concentration (AGG) are reported. The peak time of gastrin response in patients with moderate to severe antral atrophy was delayed, and the AGG values were lower than that of control, the integrated gastrin response (IGR) and the values of peak/fasting were also lower than that of control. The peak time of gastrin response in patients with mild antral atrophy and the AGG values were similar to the control values, but the values of peak/fasting and IGR were lower than the control values. This study shows that the delayed peak-time of gastrin response and the lowest or negative IGR suggest that there is atrophy of antral mucosa of patients. Thus, the meal test might be used to investigate the degree of antral atrophy.

A miniature transducer was swallowed into stomach or inserted in a channel of gastroscope to measure the intragas-tric waves. The intragastric pressure waves could be divided into normal, strong, weak and depression types. Normal wave appeared in the 36 normal persons. 76.5 percent of the cases with chronic gastritis demonstrated the dysfunction of motility. Strong wave was shown in the active stage of duodenal ulcer, while the weak or depression wave was demonstrated in gastric carcinoma. This study may help to recognize the pathophysiologic changes of gastric diseases and also demonstrate a method for choice of drugs to treat the diseases.

The authors report the G cell count in the antrum at great caverture in 10 normal subjects and 11 who suffered from chronic superficial gastritis (CSAG) and 11 cases of mild atrophic antral gastritis (CAAG) . Biopsies were obtained under the gastroscopic examination. The tissue sample was stained by PAP method, using the standard anti-gastrin (G-17) sera of gastrin-kit as the 1st antibody. As G cells are mostly located in the middle third of the glands, the G cell count was made at these area. In normal subject the G cell count was 480.64±145.27/mm², in CSAG was 491.05±117.98/mm², in CAAG was 495.13±296.28/mm². There is no significant difference between these three groups. As the lesions in these two types of antral gastritis are superficial, therefore there may be no severe damage of the G cells, so no remarkable difference can be seen. Staining the G cells by PAP method, the nucleus and granules can be seen clearly, so it is better than the fluorescent antibody method.

Twenty-three cases of Mallory-Weiss syndrome were diagnosed during January 1978 to October 1980. Twenty-two of them were visualized endoscopically (6.1% of 358 cases with acute upper GI bleeding) . The Mallory-Weiss mucosal laceration was usually induced by severe retching and vomiting, 7 had a histoy of alcohol intake. The laceration occurred mostly in gastric mucosa and usually associated with other upper GI mucosal lesion, which might lead to nausea and vomiting. Twenty-one cases with this lesion could be managed satisfactorily without operation, and Sengstaken-Blakemore tube was applied to control rapidly the bleeding in one case. Two cases had been operated on. It is emphasized that the incidence of Mallory-Weiss syndrome is rather high, and early endoscopy is the most valuable for correct diagnosis.

The IgG and IgA contents of gastric mucosa in 175 patients with diseases of stomach were measured with simple agar gel diffusion test. The results showed that IgG content in the gastric mucosa of gastric carcinoma was higher than that of benign diseases of stomach (₁ = 2.54 μg/mg tissue, ₂ = 1.58 μg/mg tissue) . There was significant difference in the mean value between the two (p<0.00l) . However, there was no difference in the mean value of IgA between gastric carcinoma and benign diseases of stomach (p>0.05) . The above data suggest that IgG quantitative measurement is of some value in the clinical diagnosis of gastric carcinoma.

⁸⁶RbCI method was used to measure the pancreatic blood flow in rats. Thirty rats were placed in each group. Group 1, pancreatitis was induced by injecting 5% sodium taurocholate-trypsin solution into the pancreatic duct. Group 2, Sham-operation served as control. Group 3, induced pancreatitis was treated with bovine pancreatic polypeptide (BPP) . The results revealed that pancreatic blood flow in the group 1 was approximately 50% and 74% more than that of the group 2 at 1 and 6 hr after injection respectively, and 29% reduced at 12 hr. Pancreatic blood flow in the group 3 was similar to the group 2 at 1 and 12 hr, but 24% increased at 6 hr. In the group 3, the pancreatic blood flow was markedly lowered than that of the group 1 at 1 and 6 hr. The pancreatic perfusion per gram of tissues was found parallel to the changes of pancreatic blood flow. These results suggest that the increased pancreatic blood flow is due to congestion in the early period of acute pancreatitis, whereas it is decreased due to failure of pancreatic microcirculation in the late period. It is speculated that BPP might lessen these pathological changes and thus the pancreas is protected.

Glucagon is one of the brain-gut peptides. Its physiological action in the brain is not yet clear. Two hours after injection of glucagon (1 μg/5 μl) into the lateral ventricles in Shay rats, the volume of gastric secretion and the gastric acid output were markedly inhibited and the plasma gastrin level was increased in a dose-dependent manner. The inhibitory action was abolished after removal of the abdominal sympathetic ganglia. This indicates that the above central effect of glucagon is affected through the sympathetic nerves. These results show that glucagon in the brain might participate in the regulation of gastric acid secretion.