gastrins and Gastric-Dilatation

To observe the effects of Herba dendrobii on rats with stomach-heat syndrome and to explore the mechanisms.. Rats were fed with decoction of Rhizoma Zingiberis for 15 continuous days to induce the model of stomach-heat syndrome. After modeling, Herba Dendrobii (HD) decoction were given (in the doses of 1.5, 0.75 g x kg(-1) respectively) for 10 days. After treatment, amount of the daily diet, volume and absorbance of urine, pellet number and moistness of excrement, color and coating degree of tongue were recorded; the body thermal effects were detected with thermal texture maps (TTM) system; the biochemical indexes of blood reflecting the physiological function of stomach, including thromboxaneB2 (TXB2), 6-keto-prostaglandin F1alpha(6-keto-PGF1alpha), motilin (MTL), gastrin (Gas), somatostation (SS), interleukin-4 (IL-4) and interleukin-8 (IL-8) were measured by radio immunoassay; and the histological changes of gastric mucosa were observed by hematoxylin-eosin (HE) stain.. The model rat had yellow coating and red tongues (P < 0.05). The amount of daily diet were increased (over 10%), urine volume and excrement pellet number were decreased (over 10%). The their urine color became deep (P < 0.01) and their excrement became dry. The temperatures in head, neck, left fore-armpit, chest, up-abdomen, mid-abdomen of the model rats were raised up (difference > 0.5 degrees C or difference > 1.0 degree C ). The content of 6-keto-PGF1alpha in blood of model rats decreased evidently (P < 0.01), and the contents of MTL, Gas and IL-8 increased conspicuously (P < 0.01). The histological changes of gastric mucosa in the model rats were as follows: diffuse congestion, infiltration of neutrophil, less secretion, decrease of the number of chief and parietal cells, etc (P < 0. 05 or P < 0.01). After treatment with HD, except the daily food weight, the temperatures in head, neck and chest, the content of MTL and the number of chief cells, the other indexes observed above were improved noticeably (difference > 0.5 RC or difference > 1.0 degree C, P < 0.05 or P < 0.01).. The reason why HD relieves the general symptom and sign the gastric mucosa of rats with stomach-heat syndrome is that HD can increase 6-keto-PGF1alpha and decrease IL-8, Gas, TXB2 in their blood.

Topics: Animals; Drugs, Chinese Herbal; Gastric Dilatation; Gastrins; Interleukin-4; Interleukin-8; Male; Motilin; Prostaglandins; Rats; Rats, Sprague-Dawley; Signal Detection, Psychological; Signal Transduction; Stomach Diseases; Syndrome; Thromboxanes

To investigate the intragastric mechanisms for regulation of gastric neuroendocrine functions during gastric distention in isolated vascularly perfused rat stomach.. Isolated vascularly perfused rat stomach was prepared, then the gastric lumen was distended with either 5,10 or 15 ml pH7 isotonic saline during a period of 20 min. During the distention, the axonal blocker tetrodotoxin (TTX), the cholinergic antagonist atropine, or the putative somatostatin-antagonist cyclo (7-aminoheptanoyl-Phe-D-Trp-Lys-Thr(Bzl)) were applied by vascular perfusion. The releases of gastrin and somatostatin were then examined by radioimmunoassay.. The graded gastric distention caused a significant volume-dependent decrease in gastrin secretion (-183+/-75 (5 ml), -385+/-86 (10 ml) and -440+/-85 (15 ml) pg/20 min) and a significant increase of somatostatin secretion (260+/-102 (5 ml), 608+/-148 (10 ml) and 943+/-316 (15 ml) pg/20 min). In response to 10 ml distention, the infusion of either axonal blocker TTX (10(-6) M) or cholinergic blocker atropine (10(-7) M) had a similar affect. They both attenuated the decrease of gastrin release by approximately 50 %, and attenuated the increase of somatostatin release by approximately 40 %. The infusion of somatostatin-antagonist cyclo (7-aminoheptanoyl-Phe-D-Trp-Lys-Thr (Bzl)) (10(-6)M) attenuated the decrease of gastrin release by about 60 %. Furthermore, combined infusion of the somatostatin-antagonist and atropine completely abolished distention-induced inhibition of gastrin release.. The present data suggest that distention of isolated rat stomach stimulates somatostatin release via cholinergic and non-cholinergic TTX-insensitive pathways. Both somatostatin and intrinsic cholinergic pathways are responsible for distention-induced inhibition of gastrin release.

Topics: Animals; Atropine; Gastric Dilatation; Gastric Mucosa; Gastrins; In Vitro Techniques; Male; Muscarinic Antagonists; Rats; Rats, Wistar; Somatostatin; Stomach; Tetrodotoxin

Helicobacter pylori infection contributes to hypergastrinemia and hypersecretion of acid by blocking inhibitory reflex pathways to gastrin and parietal cells normally activated by antral distention. Our aim was to investigate whether a similar blockade of inhibitory responses could be provoked by inducing gastritis with aspirin, thus implicating a common inflammatory component, possibly a proinflammatory cytokine(s).. We studied the effects of antral distention on stimulated acid secretion and gastrin release in H. pylori-negative volunteers, before and after 3 days of aspirin therapy (2 g daily). Immediately before the examinations, the severity of gastric mucosal injury was evaluated macroscopically and histologically, and the production of interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma was determined by immunohistochemistry.. Most subjects had severe gastric injury after aspirin therapy, resulting in a substantially increased production of IL-1beta, IL-6, and IL-8 but not of TNF-alpha and IFN-gamma in the antral mucosa. In these subjects the acid-inhibitory response was abolished or markedly reduced. Conversely, aspirin therapy failed to affect the gastrin release in all subjects studied.. The disinhibition of acid secretion in response to antral distention is a joint feature of the gastritis induced by aspirin and H. pylori infection, possibly related to the increased production of IL-1beta, IL-6, and IL-8. The H. pylori-related hypergastrinemia apparently has a different background.

Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Cytokines; Female; Gastric Acid; Gastric Dilatation; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Male; Time Factors

Helicobacter pylori infection and duodenal ulcer disease are firmly correlated. However, the bacteria do mainly colonize the antrum, indicating an indirect pathogenic mechanism. The aim of this study was to test a concept claiming that H. pylori infection of the antrum selectively blocks normal inhibitory reflex pathways to gastrin and parietal cells.. The effect of antral distention was studied on gastric acid secretion stimulated by pentagastrin and on gastrin release stimulated by gastrin-releasing peptide in H. pylori-infected and noninfected patients with and without duodenal ulcer disease, as well as after eradication of the bacteria.. The inhibitory effect on gastric acid secretion induced by antral distention was absent in H. pylori-infected patients irrespective of whether or not they had duodenal ulcer disease. The inhibitory mechanism was restituted in 8 of 10 patients within 9 months after successful eradication of H. pylori infection. Similar results were obtained in studies on gastrin release.. H. pylori infection blocks normal, physiological inhibitory mechanisms from the antrum to both the gastrin cells and to the parietal cell region, resulting in increased gastrin release and impaired inhibition of gastric acid secretion, which will probably lead to an increased duodenal acid load as a general prerequisite for the development of duodenal ulcer disease.

Topics: Adult; Aged; Duodenal Ulcer; Female; Gastric Acid; Gastric Dilatation; Gastrin-Releasing Peptide; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Parietal Cells, Gastric; Pentagastrin; Peptides; Pyloric Antrum; Stomach Diseases

Abnormal gastric motility has been suggested as a possible causative factor for acute gastric dilatation observed in nonhuman primates. To evaluate gastric motility in a colony, fasting serum gastrin immunoreactivity and gastric emptying times were assessed in rhesus monkeys that had survived single episodes of acute gastric dilatation. These were paired with age- and weight-matched control monkeys from the same colony. Neither gastric emptying times nor gastrin assays were significantly different between the acute gastric dilatation and control groups.

Topics: Acute Disease; Animals; Biomarkers; Gastric Dilatation; Gastric Emptying; Gastrins; Gastrointestinal Motility; Macaca mulatta; Primate Diseases; Reference Values

The gastrin response to a low and a high dose of gastrin-releasing peptide infusion was studied in healthy volunteers and in patients with duodenal ulcer disease. In duodenal ulcer patients, the gastrin response was exaggerated. Cholinergic blockade did not change the gastrin release in healthy volunteers. Antrum distension during neutralization of the gastric lumen was unable to stimulate gastrin release, also under cholinergic blockade. However, in healthy volunteers distension of the antrum significantly inhibited the gastrin response to gastrin-releasing peptide infusion. This inhibitory influence was most pronounced in patients given the lower dose of the neuropeptide. Cholinergic blockade counteracted the inhibitory effect exerted by antral distension. On the other hand, antral distension did not alter the gastrin response to gastrin-releasing peptide in patients with duodenal ulcer disease. These results suggest an additional defective inhibitory mechanism in duodenal ulcer patients.

Topics: Adult; Catheterization; Duodenal Ulcer; Female; Gastric Dilatation; Gastrin-Releasing Peptide; Gastrins; Gastrointestinal Hormones; Humans; Male; Middle Aged; Peptides; Pyloric Antrum; Radioimmunoassay

We report a 45-year-old woman with chronic peptic ulcer disease and multiple episodes of bowel obstruction, who was admitted with gastric outlet obstruction. Because of gastric hypersecretion, a diagnosis of Zollinger-Ellison syndrome was suspected and an initial serum gastrin of 1,251 pg/ml supported this diagnosis. Subsequent evaluation failed to reveal a gastrinoma. A repeat serum gastrin level after 14 days of continuous nasogastric decompression was 43 pg/ml, suggesting that the initial hypergastrinemia was due to antral distention. It is important to consider the possibility of gastric outlet obstruction as a stimulus for serum gastrins in the range previously considered diagnostic for the Zollinger-Ellison syndrome.

Topics: Diagnosis, Differential; Female; Gastric Dilatation; Gastrins; Humans; Intestinal Obstruction; Middle Aged; Peptic Ulcer; Pyloric Antrum; Zollinger-Ellison Syndrome

Fasting and postprandial gastroesophageal sphincter pressure (GESP) and plasma gastrin immunoreactivity were measured in 6 dogs from 9 through 60 months after treatment for and recovery from gastric dilatation-volvulus (GDV). The GESP was not significantly increased in these dogs, compared with that in clinically normal dogs in either the fasting or postprandial state. Corresponding plasma gastrin immunoreactivity was not significantly increased in dogs of the GDV-recovered group, compared with that in clinically normal dogs (fasting or postprandial). An exaggerated increase in GESP in response to food-induced gastrin release was not observed in dogs of the GDV-recovered group. Exogenously administered pentagastrin (3-micrograms/kg bolus, IV) increased fasting GESP in clinically normal dogs over a 4-minute test period (P = 0.01). Gastric distention in response to oral administration of isosmolar saline solution (500 ml) did not significantly increase GESP or plasma gastrin immunoreactivity in clinically normal dogs. In anesthetized clinically normal dogs, gastric distention in response to use of balloons filled to exert intragastric pressure of 30 mm of Hg also did not cause significant increase in plasma gastrin immunoreactivity. Increased GESP, secondary to hypergastrinemia or gastric distention, is an unlikely cause of eructation failure in dogs with GDV.

Topics: Animals; Dog Diseases; Dogs; Esophagogastric Junction; Gastric Dilatation; Gastrins; Pentagastrin; Pressure; Stomach Volvulus

Plasma gastrin immunoreactivity was measured by radioimmunoassay in 45 dogs with acute gastric dilatation-volvulus (GDV). Significant increases (P less than 0.05) were found in dogs with acute GDV and in the fasted state after surgical treatment and recovery. The data suggested that dogs that have had GDV may have preexisting high plasma gastrin immunoreactivity. In dogs with acute GDV, plasma gastrin immunoreactivity was not found to be helpful in formulating prognosis. Circumcostal gastropexy did not affect plasma gastrin immunoreactivity.

Topics: Acute Disease; Aerophagy; Animals; Dog Diseases; Dogs; Gastric Dilatation; Gastrins; Humans; Stomach Volvulus

The acid secretion from the main stomachs and from denervated Heidenhain pouches in response to peptone meals infused in the stomach was determined in 4 dogs. When expressed as percent of the maximal acid response to histamine, the acid secretion from the innervated and from the denervated fundic mucosa was similar, but the response from the Heidenhain pouch was larger when expressed as percent of the maximal response to pentagastrin. These studies indicate that, under the conditions used, short (gastrogastric) and long (vagovagal) reflexes during the gastric phase, are of minor importance in inducing the acid response to the meal.

Topics: Animals; Dogs; Gastric Acid; Gastric Dilatation; Gastric Fundus; Gastric Mucosa; Gastrins; Peptones; Reflex; Stomach; Vagotomy, Proximal Gastric

1. Distention of the vagally denervated fundic gland area, although by itself a generally ineffective stimulus to acid secretion in this study, will markedly increase the acid secretory response to stimulation by endogenous gastrin, pentagastrin and histamine. Even maximal responses to histamine can be increased, thus demonstrating true potentiation between distention and humoral stimuli. 2. The magnitude of the distention potentiation does not appear to be influenced by the nature of the background stimulus or the background level of secretion. 3. The distention potentiation of the response to histamine is reduced but not abolished by intravenous atropine and hexamethonium. Thus, there appear to be two components to the local distention mechanism. One is cholinergic, the other, atropine-resistant component is possibly non-cholinergic. At least one of these components, possibly the cholinergic, involves a nicotinic synapse in its pathway.

Topics: Animals; Atropine; Denervation; Dogs; Drug Synergism; Female; Gastric Dilatation; Gastric Juice; Gastrins; Histamine; Male; Pentagastrin; Stomach; Vagus Nerve

We evaluated whether gastric distention with saline test meals could release gastrin in healthy subjects and whether luminal acidification or atropine would modify this response. Distention with 700 ml saline adjusted to pH 5.0 led to a significant gastrin response (averaging 9 +/- 3 pg/ml above basal levels during the first 15 min after distention, P less than 0.02), whereas distention with 25 ml saline led to no gastrin release. Distention with 700 ml saline adjusted to pH 2.5 also led to a significant gastrin rise, which was nearly identical to that seen at pH 5.0. A small dose of atropine (2.3 micrograms/kg i.v.) significantly enhanced the gastrin response to 700-ml distention at pH 5.0 (average gastrin rise 20 +/- 3 pg/ml, P less than 0.02 vs. 700 ml without atropine). This enhancement of gastrin release by atropine was not due to changes in intragastric pH, because pH was held constant at 5.0 by in vivo intragastric titration. Enhancement was also not due to greater gastric distention after atropine, because gastric volumes after the 700-ml test meal were similar with or without atropine. Although atropine enhanced distention-induced gastrin release, atropine reduced acid secretion by more than 50% (P less than 0.05). Our findings indicate (a) that gastric distention releases significant amounts of gastrin in healthy subjects; (b) this gastrin response is resistant to inhibition by luminal acidification to pH 2.5 and (c) the gastrin response to distention is enhanced by atropine, suggesting that distention may also activate cholinergic pathways that inhibit gastrin release.

Topics: Adult; Atropine; Female; Gastric Dilatation; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Sodium Chloride

Plasma gastrin concentrations and gastric acid output were measured during graded balloon distention of the gastric fundus and body in 20 patients with duodenal ulcer. Acid output rose stepwise with increasing distention volumes but plasma gastrin remained unchanged. During intragastric neutralization in 5 of these subjects, fundic distention did not elicit a significant rise in plasma gastrin, whereas the acid response was similar to that observed in the control study when the gastric contents were acid. In 8 of the 20 patients, proximal gastric vagotomy profoundly suppressed the acid response to fundic distention. Basal plasma gastrin concentrations were elevated after vagotomy but were unchanged during graded fundic distention. The results suggest that neural reflex activation of the oxyntic glands is the main mechanism by which fundic distention stimulates acid secretion in man. The failure of fundic distention to release gastrin does not, however, completely rule out the existence of an oxyntopyloric distention reflex for gastrin release in man. Fundic distention in man seems to both stimulate acid secretion and induce an inhibitory mechanism acting on acid secretion. This inhibitory mechanism may, purely speculatively, also mask the effect of an oxyntopyloric reflex for gastrin release. The present study and earlier work suggest that in man distention of the stomach is a poor stimulus for release of gastrin, regardless of whether the pyloric or the oxyntic gland area, or both, are distended.

Topics: Adult; Duodenal Ulcer; Gastric Dilatation; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Pylorus; Reflex; Stomach

Topics: Animals; Dogs; Female; Fluoroscopy; Gastric Dilatation; Gastrins; Peptides; Pressure; Sodium Chloride; Stomach

Topics: Abdominal Muscles; Animals; Cell Division; Diet; Gastric Dilatation; Gastric Juice; Gastric Mucosa; Gastrins; Male; Organ Size; Pyloric Stenosis; Rats