Cow's milk intolerance with melena

The clinical features, the results of gastric secretory function tests, and the duodenojejunal morphology of six infants (aged 0.42–1.23 years) with anemia and melena considered to be due to latent cow's milk intolerance (LCMI) were compared with the findings in nine infants (aged 0.19–0.87 years) with cow's milk-induced malabsorption (CMI). The infants with LCMI had a short period of breast feeding, normal weight gain without symptoms of malabsorption, and no atopic history. The maximal acid secretion was decreased (P<0.01) and the concentration of fasting serum gastrin raised (P<0.01) compared with the controls. Gastric biopsy revealed epithelial degeneration in three and erosion in one out of four samples.The duodenojejunal biopsy revealed slight changes in two samples, the others being normal. The number of eosinophils was increased in four out of six biopsies. Although the number of intraepithelial lymphocytes was increased in LCMI the rise was not as significant as in children with CMI (P<0.05).We conclude from our results that LCMI seems to be a separate clinical entity. The determination of fasting serum gastrin, maximal gastric acid secretion and intraepithelial lymphocytes on duodenojejunal biopsy appear to be helpful in making the diagnosis.     

Immunohistochemistry and morphometry of gastrin cells in the rat pyloric antrum during starvation

Summary The gastrin cells (G cells) in the rat pyloric antrum after 7, 14, 21 and 28 days of starvation were investigated by immunohistochemistry and electron microscopy. In the peroxidase anti-peroxidase method for light microscopy, gastrin immunoreactive cells during starvation markedly decreased in number and size. Quantitative electron microscopy revealed that during starvation the number of electron-lucent granules were greatly reduced, but the number of electron-dense granules increased; the number of intermediate granules were not remarkably changed in G cells. These results may suggest that the synthesis of gastrin and granule maturation were greatly inhibited during long-term starvation.     

泰胃美用于围麻醉期呕吐误吸的防治（附30例分析）

目的　通过测定静脉注射泰胃美前后胃液 p H及血清胃泌素含量 ,探讨泰胃美对围麻醉期呕吐、误吸的防治作用。方法　选择胆囊切除手术 30例 ,随机分成实验组和对照组各 15例 ,实验组于全麻诱导前 30分钟静脉注射泰胃美 2 0 0 mg,对照组静脉注射生理盐水 2 ml。全部病人采用气静 +吸入复合麻醉 ,分别于麻醉诱导前、后 30分钟 ,抽取静脉血 2 .0 ml测定胃泌素含量及吸取胃液 5 .0 ml测定 p H值。结果　应用泰胃美前胃液 p H值为 2 .8± 0 .5 ,而用泰胃美后 30分钟胃液 p H上升为 4.5± 0 .6 (P<0 .0 1)。应用泰胃美前血清胃泌素含量为 138.5 6± 5 6 .38(pg/ ml) ,而用泰胃美 30分钟后为 111.6 0± 45 .6 (P<0 .0 1)。结论　应用泰胃美可使胃酸和胃泌素分泌下降 ,胃液 p H值迅速增高 ,可达 4.0以上。对预防呕吐、误吸及误吸性肺炎、呼吸衰竭具有一定意义     

大鼠实验性胃溃疡自愈期间胃窦粘膜G、D细胞变化的免疫组织化学研究

本实验用成年雄性Wistar大鼠53只,分为溃疡组、盐水对照组和正常对照组。在手术后4、10,14、21及28天分批取材。用Sternberger PAP法进行免疫组织化学染色,分别显示胃窦粘膜胃泌素细胞(G细胞)和生长抑素细胞(D细胞),观察大鼠实验性胃溃疡自愈期间,G和D细胞的形态变化,并进行了细胞计数和统计学分析。本文结果表示,溃疡组G细胞数量在术后10至14天明显增多(P<0.01),21、28天趋于减少,但仍高于对照组。有些G细胞排列成群,密集呈明显带状。正常时G细胞分布在幽门腺的中、下1/3处,而溃疡组可见有些G细胞分布在腺的上部。D细胞数量仅在术后10天增多(P<0.01),与正常对照组相比差异显著。用免疫组织化学双重染色法,可见G细胞和D细胞之间存在着形态上的接触。溃疡自愈期间,G/D细胞比值未见明显改变。本实验结果提示,胃窦粘膜局部G、D细胞的变化和大鼠实验性胃溃疡自愈修复之间有着一定的联系。     

Bombesin microinfusion into the paraventricular nucleus suppresses gastric acid secretion in the rat

Bombesin is a particularly potent inhibitor of gastric acid secretion when injected intracisternally in the rat. Because bombesin-like immunoreactivity is found in several forebrain regions implicated in gut regulation, the ability of bombesin to affect gastric secretion was tested in these areas by direct microinfusion. Bombesin significantly and dose-relatedly suppressed gastric acid secretion when it was infused into the hypothalamic paraventricular nucleus. Bombesin microinfusion into the ventromedial or lateral hypothalamic areas, or the caudate-putamen, had no significant effect. A further experiment using glass micropipets showed that back-diffusion of bombesin along the cannula track to a distant site of action was unlikely to account for the results obtained, and provided further evidence that the active site is limited to the paraventricular nucleus and possibly the ventralmost nucleus reuniens. The results suggest that the bombesin receptors and immunoreactive terminals previously identified in this region may be involved in the central regulation of gastric secretion.     

Role of circulating catecholamines in the control of pancreatic polypeptide and gastrin release

The influence of circulating catecholamines on the release of pancreatic polypeptide (PP) and gastrin was studied in volunteers. Physical exercise increased plasma epinephrine by 374 +/- 123% and plasma norepinephrine by 167 +/- 30%, but plasma PP concentrations remained unchanged during standardized bicycle ergometry. Immediately after cessation of exercise catecholamine levels decreased rapidly, whereas PP concentrations increased by 55%. In a second series, epinephrine infusion (5, 25, and 75 ng.kg-1.min-1) increased epinephrine levels by 38 +/- 12, 331 +/- 69, and 1229 +/- 131%, respectively, whilst norepinephrine was unaffected. Neither during nor after catecholamine infusion PP secretion was affected. Gastrin release increased by a maximum of 85 +/- 38% (at epinephrine 75 ng.kg-1.min-1). It is concluded, that (1) changes in circulating adrenaline do not significantly influence PP secretion in man; (2) the PP increase immediately following physical exercise cannot be attributed to a rapid fall of catecholamine levels; (3) endogenous catecholamines are of minor importance in the control of gastrin secretion.     

轮状病毒性肠炎患儿空腹血清胃泌素胃动素水平的研究

目的探讨轮状病毒性肠炎患儿空腹血清胃泌素、胃动素水平的改变.方法用放射免疫分析法分别测定45例婴幼儿轮状病毒性肠炎和16例健康对照者空腹血清胃泌素、胃动素的浓度.结果婴幼儿轮状病毒性肠炎急性期空腹血清胃泌素、胃动素浓度高于恢复期及对照组,差异有显著性意义,p＜0.01.结论胃泌素、胃动素可能参与了轮状病毒性肠炎的发病机制.     

消化性溃疡,胃癌患者胃窦粘膜中胃肠激素含量变化及其意义

研究了胃十二指肠疾病患者胃窦粘膜胃泌素（Ｇａｓ）、生长抑素（ＳＳ）、Ｐ－物质（ＳＰ）的含量变化及其意义。结果表明：胃窦粘膜ＳＳ含量在胃溃疡组低于其余各组（Ｐ均〈０．０５），而在胃癌时则显著增高（Ｐ〈０．００１）；ＳＰ浓度在十二指肠溃疡组显著低于其余各组（Ｐ均〈０．０５）；胃癌患者Ｇａｓ水平显著高于对照组（Ｐ〈０．０５）；ＳＳ与ＳＰ在十二指肠溃时呈明显负相关。提示：胃粘膜中Ｇａｓ、ＳＳ、ＳＰ的含量变     

The Role of the Beta-Adrenergic Receptor in the Secretion of Gastrin: Studies in Normal Subjects and in Patients with Duodenal Ulcers

Intravenous infusion of isoproterenol, a beta-adrenergic receptor stimulatory agent, increased serum gastrin concentration significantly more in patients with a duodenal ulcer than in healthy subjects. The rise in pulse rate, blood glucose concentration and in serum insulin was the same in both groups of subjects. Gastrin secretion was also increased significantly more in the patients than in the control subjects after a beef-meal. Basal serum gastrin concentrations were higher in the patients than in the control subjects and correlated to the rise in serum gastrin during both tests in the patients with a duodenal ulcer. Isoproterenol and meal stimulated gastrin secretion, expressed as percent of the basal value, were twice as high in the patients as in the control subjects. The combined administration of isoproterenol and the meal had an additive effect on the rise in serum gastrin. Isoproterenol stimulated gastrin secretion was completely suppressed by propranolol, a beta-adrenergic receptor blocking agent, which had no effect on meal stimulated gastrin secretion. It is concluded that the mechanism of the hypersecretion of gastrin in patients with a duodenal ulcer did not involve a specific abnormality of the beta-adrenergic receptor or the receptor which recognized proteins and their digested products. There is no established role of beta-adrenergic receptor activity in the hypersecretion of gastrin in patients with duodenal ulcers. It is suggested that the beta-adrenergic receptor may have some yet unknown function unrelated to the acute secretory response of gastrin.     

The effect of gastrin on basal and aminoacid-stimulated insulin and glucagon secretion in man

Abstract. The effect of gastrin on basal and aminoacid-stimulated glucagon and insulin secretion was studied in eleven normal young subjects. The concentrations of glucagon, insulin and gastrin in plasma or serum were measured radioimmunochemically. The results of amino-acid-stimulation were compared to those obtained during a protein-rich meal.
Intravenous injection of synthetic human gastrin-17 in doses from 15.6 ng to 1 μg/kg increased the concentration of glucagon and insulin in peripheral venous blood to a maximum within 5 min. In spite of the enhanced concentrations of insulin induced by gastrin, corresponding concentrations of glucose were either unchanged or increased. Infusion of a mixture of fifteen aminoacids increased the concentrations of glucose, glucagon and insulin. While the increases in glucose and insulin concentrations were similar to those obtained after a protein-rich meal, the glucagon response was much larger after the infusion. Injection of gastrin-17 after 30 min of infusion of aminoacids did not potentiate either the glucagon or the insulin response.
The results indicate that gastrin, besides stimulating insulin secretion, can also stimulate glucagon secretion in a dose-dependent manner. The concentrations of gastrin necessary to stimulate glucagon secretion significantly correspond to the concentrations found in diseases with endogenous hypergastrinaemia (achlorhydria and Zollinger-Ellison syndrome). While gastrin potentiates the glucose-induced insulin secretion, it does not potentiate neither the aminoacid-induced insulin nor glucagon secretion.