The protective action of the organic substances in naftusia water on erosive-ulcerative lesions of the gastric mucosa in rats undergoing immobilization-cold stress

It is shown that 7-11-day long consumption (by rats) of water naftusia or organic matters isolated from it which contain carbonic acids and catecholamines possessing paramagnetic activity exerts a preventive effect on stress injuries of the mucous membrane of the stomach. Gastric protective action of naftusia goes with hyperplasia and hypertrophy of argyrophil endocrinocytes and antral mucosa, with an increase of gastrin content in it as well as in blood serum, shortening of the nembutal sleep duration.     

吗啡和纳洛酮对损毁下丘脑诱致的大鼠胃粘膜损伤之影响

本实验观察了静注吗啡和纳洛酮对电解损毁后部下丘脑诱致的大鼠胃粘膜损伤的影响并观察了在静注吗啡、纳洛酮后和侧脑室注射纳洛酮后其胃酸分泌和血清胃泌素水平之变化。实验揭示,吗啡仅略为降低该神经源性胃粘膜损伤程度,而纳洛酮则明显地减少其胃粘膜损伤;静注吗啡能抑制后部下丘脑损毁后大鼠的胃酸分泌,增加其血清胃泌素水平,而静注纳络酮后,这种大鼠的胃酸分泌增加,但血清胃泌素水平无明显变化;侧脑室注射纳洛酮对后部下丘脑损毁后大鼠胃酸分泌和血清胃泌素水平无明显影响。本结果表明,胃酸可能是导致这种消化道损伤的条件之一,而不是最重要因素;静注纳洛酮对后部下丘脑损毀后大鼠胃粘膜变化有保护作用。后者提示,内源性阿片样肽可能参与这种神经源性胃粘膜损伤的形成。     

The role of food intake on gastric mucosal growth and gastrin receptors during pregnancy and lactation

We examined the effects of pregnancy and lactation on mucosal growth and the numbers and affinity of gastrin receptors in the oxyntic gland mucosa in rats and compared these with changes in serum gastrin levels and food consumption. Gastric mucosal DNA, RNA, and protein contents were significantly increased during lactation. These changes were not observed in either pregnant or nonlactating rats which had given birth at the same time as the lactating animals. The gastrin-binding capacity of a membrane fraction of the oxyntic mucosa was also increased at the corresponding periods in lactating rats (Days 7, 15, 20). Scatchard plot analysis revealed that the number of gastrin receptors was significantly increased without any change in affinity. Food consumption and levels of serum gastrin remained unaltered in pregnant and non-lactating rats compared to virgin controls, but were significantly increased in lactating rats. Increased serum gastrin levels and gastrin binding capacities in lactating rats (Day 15) were abolished by preventing increased food consumption by means of pair feeding. The results demonstrate that the number of gastrin receptors in the oxyntic mucosa increases during lactation in rats. This increase is probably due to hypergastrinemia caused by increased food intake. The increased number of gastrin receptors may be involved in the mechanism of hypertrophic responses of the gastric mucosa in lactating rats.     

Protective action of pantetine on the denervated stomach

Bilateral subdiaphragmal vagotomy was performed in sexually-mature Wistar male rats. To prevent neurodystrophic processes in the stomach mucous membrane some animals were injected pantetine subcutaneously at a dose of 30 mg/kg 5 times daily for 10 days. Pantetine injected to vagotomized animals decreased destructive lesions in the stomach mucous membrane. Enhanced biosynthesis and the inhibition of gastrin and serotonin release from G and Ec cells respectively have been observed. The results obtained substantiate the use of pantetine for the pharmacological correction of postoperative complications in patients after vagotomy.     

Autoradiographic demonstration of gastrin binding sites in rat gastric mucosa

The location of 125I-iodotyrosyl gastrin I binding sites in rat gastric mucosa was studied. Peptide specificity was demonstrated by competitive binding studies through the addition of a large dose of cold human gastrin I or cholecystokinin-octapeptide. Autoradiography of the stomach tissue was carried out by freeze-drying, embedding in Epon, wet-sectioning with ethylene glycol, and dry-mounting the emulsion film by means of the wire-loop method to prevent loss of the labeled substance. Specific binding sites for gastrin were found on parietal and chief cells, whereas few binding sites were seen on the surface mucous or mucous neck cells. Binding sites on the parietal cells were dispersed in the cytoplasm, while those on the chief cells were found near the basal plasma membrane.     

交感神经对去迷走神经大鼠胃泌素释放的刺激作用

为了探讨迷走神经切除后血清胃泌素浓度增加的机制,本实验用放射免疫法系统观察了大鼠双侧膈下迷走神经切除后三个月血清胃泌素浓度的变化和交感神经在这种变化中的作用。结果发现,迷走神经切除后,血清胃泌素浓度增加6倍以上,而且这种增加不是继发于胃内pH和胃内压的改变;迷走神经和交感神经都切除的动物,血清胃泌素浓度也有增加,但明显低于单纯迷走神经切除组;迷走神经切除后两个月再切除交感神经可使已升高的胃泌素下降42％。实验说明,迷走神经切除后,交感神经可刺激胃泌素释放,这一作用是去迷走神经后血清胃泌素水平增加的原因之一。     

血清胃泌素变化与急性胃粘膜病变关系的研究

对大白鼠血清中胃泌素水平的变化与急性胃粘膜病变的关系进行了初步的研究,结果表明以消炎痛为诱因引起的急性胃粘膜病变大白鼠血清胃泌素水平明显增高。而维酶素可以抑制因消炎痛引起的急性胃粘膜病变时血清胃泌素的释放,对胃粘膜具有保护作用。     

Sex-related difference in antral and serum gastrin levels in the rat.

Antral and serum gastrin concentrations were found to be significantly lower in female than in male rats. Following ovariectomy, serum gastrin concentration significantly increased to male levels; tissue gastrin also increased, but not significantly. Daily injections of estradiol benzoate (2 mug/day) abolished the rise in gastrin levels after ovariectomy. Antral and serum gastrin concentrations were significantly higher in lactating rats than in any other group tested. The possible relationships among sex-dependent changes in food intake, gastrin concentration, and gastric secretion are discussed.     

Role of the mucous barrier in the pathogenesis of stress ulcers of the stomach

Using the model of immobilizing stress in rats, it has been established that the content of sialic acids in the stomach mucous membrane (SMM) and blood serum rises with simultaneous activation of proteolytic enzymes in them. The preliminary adaptation to short stressor influences parallel with an antipathogenic effect normalizes the content of sialic acids in the blood serum and SMM. The conclusion is made on the essential role of the degradation of gastric mucus in pathogenesis of stress ulcers.     

Remodeling of the Residual Gastric Mucosa after Roux-En-Y Gastric Bypass or Vertical Sleeve Gastrectomy in Diet-Induced Obese Rats

Whereas the remodeling of intestinal mucosa after bariatric surgeries has been the matter of numerous studies to our knowledge, very few reported on the remodeling of the residual gastric mucosa. In this study, we analyzed remodeling of gastric mucosa after Roux-en-Y gastric bypass (RYGB) and vertical sleeve gastrectomy (VSG) in rats. Diet-induced obese rats were subjected to RYGB, VSG or sham surgical procedures. All animals were assessed for food intake, body-weight, fasting blood, metabolites and hormones profiling, as well as insulin and glucose tolerance tests before and up to 5 weeks post-surgery. Remodeling of gastric tissues was analyzed by routine histology and immunohistochemistry studies, and qRT-PCR analyses of ghrelin and gastrin mRNA levels. In obese rats with impaired glucose tolerance, VSG and RYGB caused substantial weight loss and rats greatly improved their oral glucose tolerance. The remaining gastric mucosa after VSG and gastric pouch (GP) after RYGB revealed a hyperplasia of the mucous neck cells that displayed a strong immunoreactivity for parietal cell H⁺/K⁺-ATPase. Ghrelin mRNA levels were reduced by 2-fold in remaining fundic mucosa after VSG and 10-fold in GP after RYGB. In the antrum, gastrin mRNA levels were reduced after VSG in line with the reduced number of gastrin positive cells. This study reports novel and important observations dealing with the remaining gastric mucosa after RYGB and VSG. The data demonstrate, for the first time, a hyperplasia of the mucous neck cells, a transit cell population of the stomach bearing differentiating capacities into zymogenic and peptic cells.     

Ciprofibrate stimulates the gastrin-producing cell by acting luminally on antral PPAR-alpha

The lipid-lowering drug ciprofibrate stimulates gastrin-producing cells in the rat stomach without lowering gastric acidity. Although suggested to be a luminal action on antral peroxisome proliferator-activated receptor-alpha (PPAR-alpha), the mechanism is still not fully elucidated. Gastric bypass was surgically prepared in male Sprague-Dawley rats. Gastric-bypassed and sham-operated rats were either given ciprofibrate (50 mg.kg(-1).day(-1) in methocel) or vehicle alone for 7 wk. PPAR-alpha knockout (KO) and wild-type (WT) mice were either given ciprofibrate (500 mg.kg(-1).day(-1) in methocel) or vehicle alone for 2 wk. The concentration of gastrin in blood was analyzed. Antral G cell density and gastrin mRNA abundance were determined by using immunostaining and Northern blot analysis. Ciprofibrate did not raise plasma gastrin or G cell density in gastric-bypassed rats, although the gastrin mRNA level was slightly increased. In contrast, ciprofibrate induced hypergastrinemia, a 50% increase in G cell density, and a threefold increase in gastrin mRNA in sham-operated rats. In PPAR-alpha KO mice, ciprofibrate did not raise G cell density or the gastrin mRNA level. The serum gastrin level was reduced by ciprofibrate. In WT mice, ciprofibrate induced hypergastrinemia, a doubling of G cell density, and a threefold increase in gastrin mRNA. Comparing animals dosed with vehicle only, PPAR-alpha KO mice had higher serum gastrin concentration than WT mice. We conclude that the main effects of ciprofibrate on G cells are mediated from the antrum lumen, and the mechanism is dependent on PPAR-alpha. The results indicate that PPAR-alpha may have a role in the physiological regulation of gastrin release.     

Effect of exogenous serotonin on intragastric pH and its influence on serum gastrin levels in rats.

The effect of various doses of serotonin on the serum gastrin levels and intragastric pH in rats, was studied. After serotonin administration of 10 mg/kg i.p., a significant increase in serum gastrin levels was noted, as well as a strong increase in the intragastric pH. It was also observed that a lower dose, 5 mg/kg i.p., significantly increased serum gastrin levels, while intragastric pH was not affected, remaining at baseline values throughout the study. These results suggest that the increase observed in serum gastrin levels after administration of exogenous serotonin is not mediated by increase in intragastric pH.     

Insulinotropic and gastrin-releasing action of gastrin-releasing peptide (GRP)

The effect of intravenous administration of gastrin-releasing peptide ( GRP ) on serum gastrin and insulin levels was studied in ad libitum fed and 24-h fasted rats. Administration of GRP (55 micrograms/kg body weight) caused a significant (P less than 0.05) elevation in serum gastrin levels at 10, 30, 60, and 120 min in the rats fed ad libitum, whereas in the fasted rats, gastrin levels rose significantly only at 10 min. GRP did not cause insulin release in fasted rats, but in the fed rats, it led to a significant elevation in serum insulin levels at 10 and 30 min, in comparison to controls. GRP appears to have an insulinotropic action in addition to a gastrin-releasing effect.     

Gastrin and the ultrastructure of G cells after stimulation with acetylcholine

The effect of intragastric administration of acetylcholine on serum and antral gastrin concentrations of rats has been examined using a radioimmunoassay and quantitative electron microscopy. Exposure of the stomach of rats, previously fasted for 24h, to 2% acetylcholine for either 0.5 or 2h resulted in a significant 4--5 fold increase in serum gastrin concentrations to levels similar to those found in fed animals. Such treatment produced no detectable change in antral gastrin concentration or in the number or electron density of secretory granules in the G cells. This lack of detectable change in the G cells was not unexpected since our calculations suggest that less than 10% of the total gastrin stored in the antrum is released over 2h as a result of the stimulation with acetylcholine. The proportion of electron-lucent secretory granules was, however, markedly increased by prolonged fixation in aldehydes. The increase was similar in both ACh stimulated and control animals. These results indicate that the ultrastructural appearance of G cell secretory granules in influenced far more by the conditions of fixation than by the release of gastrin. They therefore cast considerable doubt on the hypothesis that gastrin is released by molecular dispersion from the granules.     

Features of gastrin reaction in rats with different susceptibilities to gastric mucosa lesions in immobilization-cold stress]

The connection between the character of gastrin and acid reactions and visible morphological changes of gastric mucosa in immobilising-cold stress was studied in the experiments on mongrel rats. It is established that in the rats the fundal gastric mucosa is resistant to the disturbing action of the immobilising-cold stress. The post-stress gastrin contents in the antrum and duodenum mucosa is higher and in the serum lower than in rats with ulceration. The rats with the stress erosions have the intermediate position. The acid factor didn't play the significant role in the ulcerogenesis because its value didn't overstep the limits established in the extradigestive period.     

Serum gastrin and gastric enterochromaffin-like cells during estrous cycle, pregnancy and lactation, and in response to estrogen-like agents in rats

Histamine-containing enterochromaffin-like (ECL) cells are numerous in the gastric mucosa. They operate under the control of gastrin. ECL-cell tumors (gastric carcinoids) may arise as a consequence of sustained hypergastrinemia. For reasons unknown, such tumors have a female preponderance both in laboratory animals and humans. The present study consisted of four experiments exploring the possibility that gender-related factors might affect rat ECL cells. 1) A gender difference in terms of serum gastrin concentration and oxyntic mucosal histidine decarboxylase (HDC) activity appeared in Sprague-Dawley but not Wistar rats. Ultrastructural appearance of the ECL cells did not differ between genders. 2) During the different phases of the estrous cycle, the serum gastrin concentration, HDC activity and histamine concentration did not change. 3) During pregnancy, the serum gastrin concentration was suppressed, while it was increased during lactation. The HDC activity and the histamine concentration of the oxyntic mucosa were correlated with the levels of circulating gastrin. 4) Twelve-month treatment with estrogen-like agents, dieldrin and/or toxaphene (alone or in combination) was without any effect on the ECL cells neither in male nor in female rats. In conclusion, the ECL cells are under the control of gastrin, but probably not hormones that involve in the estrous cycle and pregnancy and lactation in rats. Possible gender-related factors behind the female preponderance of ECL-cell tumors remain unknown.     

Serum triiodothyronine and thyroxine levels in children with celiac disease]

The study was aimed at determining relationship between thyroid function and the type and degree of malabsorption. Serum triiodothyronine (T3) and thyroxine (T4) levels were determined in children with celiac disease and the secondary malabsorption. Hundred fifty five children aged between 6 months and 7 years were followed up 3 years. Coeliac disease was diagnosed with classic Interlaken criteria. All children were divided into three groups: group I--57 children aged between 6 months and 3 years with suspected celiac disease; group II--55 children aged between 2.5 and 6 years after gluten-free diet therapy; group III--52 children aged between 3 and 7 years after gluten provocation test. Serum T3 and T4 levels for each group were compared with those in children with normal gut mucous membrane. Blood serum T3 and T4 were assayed with OPIDI kit (manufactured in Swierk). Serum T4 levels were significantly lower in children with mucous membrane atrophy in comparison with dystrophic children and normal gut mucous membrane. Both serum T3 and T4 were significantly lowered in the youngest children upto 12 months of life with mucous membranes atrophy. Serum T3 and T4 concentrations were below the normal values in 4 youngest children. Blood serum T3 and T4 levels did not depend on the morphology of the intestinal villi in children treated with gluten-free diet (some children did not observe the diet and had atrophic lesions to the mucous membrane of the small intestine). Blood serum T3 level was relatively increased in children of group II with mucous membrane regeneration; in comparison with the value determined in the period of active disease.     

异麦芽低聚糖对D-半乳糖致衰老大鼠肠道菌群、血清IgG和肠黏膜sIgA的影响

目的探讨异麦芽低聚糖对D-半乳糖致衰老大鼠肠黏膜功能的影响。方法Wistar大鼠随机分为3组：（1）青年对照组,（2）衰老对照组,（3）衰老观察组（衰老＋异麦芽低聚糖）。采用D-半乳糖造成衰老模型后,应用异麦芽低聚糖灌胃,检测各组肠道菌群、血清IgG和肠黏膜sIgA。结果D-半乳糖致衰老大鼠肠道菌群失调;灌胃异麦芽低聚糖后,衰老大鼠肠道双歧杆菌增加（P〈0．05）,肠杆菌和肠球菌数量减少（P〈0．05）;血清IgG、肠黏膜sIgA含量增加（P〈0．05）。结论异麦芽低聚糖可改善衰老机体肠黏膜功能。     

Immunologic and electrophoretic detection of an epidermal chalone-containing complex in tissues of different origin]

The rabbit antiserum to one of the components of the tissue-specific protein complex isolated from the back skin of rats and containing G1- and G2-chalones was obtained. By means of this antiserum an antigen identical to the cutaneous one was found in the mucous membrane of the tongue, oesophagus, prestomach and vagina, in the epidermis of the tail and sole. The cornea, mucous membranes of the urinary bladder and intestine, liver, kidney and blood serum do not contain this antigen. According to data of disc-electrophoresis in 5%-polyacrilamide gel, the 55--81% alcohol extracts of the investigated tissues of the epidermal type, including the cornea and mucous membrane of the urinary bladder, are of similar quantitative and qualitative composition, different from that of tissues of other origin.     

A clinico-physiological study of the mechanism of the cholecystokinetic action of medicinal mineral waters of the naftusia type]

It is stated that the cholecystokinetic action of curative waters of naftusia type is due to the interaction of its organic substances, particularly bitumens, with mucous membrane of gastroduodenal zone by the intramural reflex mechanism with participation of humoral factor. It is indicated by attenuation or suppression of the effect by pharmacons interrupting the work of interchemoreception, N- and M-cholinoreceptors, beta-adrenoreceptors; intensification of the effect by blockade of alpha-adrenoreceptors; its reversion by nonselective stimulation of adrenoreceptors; release of gastrin, glucagon and insulin into blood.