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Extrinsic origin of the capsaicin-sensitive innervation of rat duodenum: possible involvement of calcitonin gene-related peptide (CGRP) in the capsaicin-induced activation of intramural non-adrenergic non-cholinergic neurons.

Capsaicin produces a concentration-related relaxation of the longitudinal muscle of the rat isolated duodenum in the presence of atropine (3 microM) plus guanethidine (3 microM). This effect of capsaicin is partly (about 40%) antagonized by tetrodotoxin (1.0 microM) suggesting the involvement of intramural non-adrenergic non-cholinergic (NANC) neurons. The capsaicin-induced relaxations are unaffected by previous bilateral vagotomy or removal of the inferior mesenteric ganglion but are completely prevented by removal of the coeliac ganglia plus the superior mesenteric ganglion (72 h before). Acute duodenal denervation did not modify the response to capsaicin. Unlike various neuropeptides (substance P, kassinin, neurokinin A, cholecystokinin octapeptide, somatostatin, vasoactive intestinal polypeptide) only the calcitonin gene-related peptide (CGRP) closely mimicked, both qualitatively and quantitatively, the capsaicin-induced relaxations. The CGRP-induced relaxations were unaffected by hexamethonium and partly reduced (about 40%) by tetrodotoxin. In preparations desensitized to adenosine-triphosphate (ATP) a putative NANC inhibitory neurotransmitter of the rat duodenum, the effects of CGRP were reduced (about 30%) as compared to controls. After ATP-desensitization tetrodotoxin did not produce any further reduction of the CGRP-induced relaxations suggesting the involvement of endogenous ATP in the neuronal (tetrodotoxin-sensitive) component of the CGRP-induced relaxations. Either ATP- or CGRP-desensitization reduced (about 50 and 65% respectively) the amplitude of the capsaicin-induced relaxations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

Regulation of Na-dependent phosphate influx across the mucosal border of duodenum by 1,25-dihydroxycholecalciferol.

Animals teated with disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP), at doses which decrease the renal production and/or the plasma levels of 1,25-dihydroxycholecalciferol [1,25(OH)2D3], display a reduced net absorption of phosphate. In this study we investigated whether EHDP-treatment and administration of 1,25(OH)2D3 to EHDP-treated animals affected the phosphate influx across the mucosal border of rabbit duodenum. The initial rate of phosphate influx into mucosal cells was measured in isolated intestine. In control, untreated rabbits, the phosphate influx shows a saturable, Na-dependent component and a diffusional, Na-independent uptake. In tissue from rabbits treated for 3 days with EHDP, the phosphate influx was found to be strongly reduced. EHDP-treatment decreased the Na-dependent, carrier mediated phosphate influx in duodenum. Administration of 1,25(OH)2D3 to EHDP-treated animals reversed the reduced phosphate influx. These effects were mainly apparent through changes in the J(mc)(max) of the phosphate influx, which was decreased from 211 +/- 38.7 nmol/cm2h in controls to 42.1 +/- 18.1 nmole/cm2 h in the EHDP-treated group and increased to 413 +/- 43.6 nmole/cm2 h by 1,25(OH)2D3. The treatment did not appear to affect the diffusional, Na-independent phosphate influx. EHDP-treatment did not affect the influx of alanine in this segment suggesting that EHDP-treatment affects only 1,25(OH)2D3-dependent transport mechanisms. The results suggest that 1,25(OH)2D3 modulates the number of carrier sites available at the mucosal membrane for Na-dependent phosphate entry.

Animals↗

Ultrastructural localization of cholecystokinin in endocrine cells of the dog duodenum by the immunogold technique.

Cholecystokinin (CCK) has been localized by the immunogold technique in a type of endocrine cell of the dog duodenum characterized by small (166 +/- 38 nm) secretory granules with fairly dense, homogeneous core separated from its enveloping membrane by a thin clear space. The CCK cell is immunocytochemically distinct and cytologically different from other types of endocrine cells, as the secretin, GIP and motilin cells, already identified in the dog duodenum.

Animals↗

Fluid secretion in the duodenum and intestinal handling of water and electrolytes in Zollinger-Ellison syndrome.

The slow marker perfusion technique was used in five patients with the Zollinger-Ellison syndrome in order to determine the basal and postcibal flow rates of fluids passing the duodenojejunal junction and distal ileum, and the composition of those fluids. Fecal water and electrolyte excretions were also measured. The 24-hr outputs at the ligament of Treitz were markedly increased, while fecal losses were normal or only slightly increased. Thus, the overall intestinal reabsorption of water was 96%. Fasting rates of fluid and electrolyte flow at the ligament of Treitz were also measured during a basal period, followed by a period of continuous gastric aspiration. Removal of gastric secretion had the following effects on the fluid passing through the duodenum: (1) dramatic decrease in flow rate; (2) an increase in osmolality, from hypotonicity to isotonicity; (3) rise of pH, from acid to alkaline values; (4) a decrease of PCO2, from high to normal values. No increase in fasting plasma levels of immunoreactive secretin and motilin was observed in Zollinger-Ellison syndrome, whereas normal subjects respond to acid in the duodenum by a marked rise in the circulating levels of these hormones. These facts suggest that, in Zollinger-Ellison syndrome: (1) the ability of the small bowel and colon to reabsorb water and electrolytes is normal: (2) duodenal dissipation of hydrogen ions is mainly due to intraluminal neutralization by bicarbonate; and (3) stimulation of water and electrolyte secretion by the pancreas is inadequate.

Adult↗

Localization of neurons innervating the upper portion of the duodenum in the motor nucleus of the vagus nerve.

Using the method of the retrograde axonal transport of horseradish peroxidase and a microelectrode technique, a population of neurons sending axons to the upper portion of the duodenum was identified in the dorsal motor nucleus of the vagus nerve. It was established that the maximal number of such neurons was located 1.0-2.5 mm rostral to the obex. The effects of their stimulation on the electrical activity of the smooth muscles of the duodenum was studied.

Animals↗

Different mechanism of magnesium and calcium transport across rat duodenum.

Concentration and voltage dependence of Mg transport across the rat duodenum was measured in an Ussing chamber. Mucosa (m) to serosa (s) Mg flux exhibits a cellular fraction comparable to that found for Ca. Mg sm flux is purely diffusive and probably restricted to the paracellular pathway. At all concentrations between 0.5 and 5 mmol/liter, Mg is secreted. Diffuse sm Mg flux is 3.5 times higher than the diffusive component of ms Mg transport. This prevalence of diffusive sm Mg flux over that from mucosa to serosa, which may be explained by an "anomalous solvent drag effect," is responsible for the Mg secretion observed. Mg 5 mmol/liter decreases ms Ca flux and abolishes Ca absorption. The voltage clamp experiments reveal that Mg has no effect on the cellular transport but only decreases diffusive ms Ca flux. 1 alpha,25-dihydroxyvitamin D3 has only a small effect on cellular Mg transport but remarkably stimulates ms Ca flux and increases Ca absorption by about 85%. Dexamethasone increases ms Mg flux but decreases ms Ca transport and hereby abolished Mg secretion or Ca absorption. In conclusion, Mg is secreted across the short-circuited duodenum whereas Ca is absorbed. There is evidence that both earth alkalines are transported by distinct cellular mechanisms. The data also demonstrate that diffusive movement across the paracellular pathway plays an important role on net Mg transport.

Animals↗

Bile exclusion from the duodenum. Its effect on gastric and pancreatic function in the dog.

The effect of diverting bile from the duodenum in four dogs with cholecystojejunostomy was studied using a double-marker perfusion technique. After the diversion procedure, a liquid meal increased acid secretion from 0.8 mmol H+/min to 1.48 mmol H+/min (P less than 0.05, paired t test); there was an associated rise in serum levels of gastrin 120 min after feeding (P less than 0.001, paired t test). Pancreatic secretion of trypsin decreased from 3.91 IU/min to 2.66 IU/min after bile diversion (P less than 0.01, paired t test), and the level of CCK was significantly lower 60 min after feeding (P less than 0.05, paired t test). There was no significant change in the rate of gastric emptying after bile diversion, but the pH of duodenal contents was lower in the later stages of digestion. These changes may explain the reported increase of peptic ulcer after diverting bile from the duodenum, and the procedure should not be considered unless the consequences of acid hypersecretion and pancreatic inhibition have been anticipated.

Amylases↗

Intestinal motility after infusion of arachis oil into duodenum and ileum of dogs.

Arachis oil and a mixture of arachis oil with bile and pancreatic enzymes were infused into the duodenum and ileum of dogs via surgically positioned catheters in order to study the mechanism of disruption of the migrating complex by intraluminally infused triglycerides, the importance of cholecystokinin and neurotensin in this event, and the pattern of digestive myoelectrical activity during fat digestion. When infused into the duodenum both arachis oil and the oil-bile-pancreatic enzyme mixture disrupted the migrating myoelectric complex (MMC). When infused into the ileum, only the oil-bile-pancreatic enzyme mixture disrupted the MMC. The duration of the disruption lasted as long as when the same amount of oil was administered orally. Triglyceride-induced digestive activity was characterized by the frequent alternation of short periods of spiking activity and short periods of quiescence. It is concluded that the triglyceride-induced disruption of the MMC-pattern is not caused by the triglyceride itself but by some emulsion or digestion product. We further suggest that the disruption is hormonally mediated and due to fat-stimulated neurotensin, rather than cholecystokinin (CCK), release.

Administration, Oral↗

Release of avian pancreatic polypeptide by various intraluminal contents in the stomach, duodenum, or ileum of turkeys.

Pancreatic polypeptide (PP) has been shown to be released postprandially in several species. In this study we tested the efficacy of an amino acid solution (905 mOsM), 0.1 N HCl (300 mOsM), 905 mOsM NaCl, 300 mOsM glucose, corn oil, and balloon distention within the stomach, duodenum, or ileum in stimulating release of avian PP (APP) in turkeys. Although they differ in osmolarity, and are thus difficult to compare, amino acids appeared to be the best stimulant and HCl the next best. The stomach was the site in which nutrients were most likely to stimulate APP release. There was no significant difference between the responsiveness of the the ileum and duodenum. A control experiment in which blood was drawn but no intraluminal treatments were administered indicated that handling and bleeding caused depression of normal fasting plasma [APP].

Amino Acids↗

Exogenous prostaglandin protects against acid-induced deep mucosal injury by stimulating alkaline secretion in rat duodenum.

In the anesthetized rat, exogenous acid (0.1-0.3 N HCl) perfused through the duodenum produced a dose-related increase in the severity of duodenal villous injury. Increasing the duration of perfusion of the 0.1 N HCl also increased the severity of the injury. The increase in the severity of the lesion score was due to an increase in the percentage of villi with damage extending to the lower half of the villus. 16,16-Dimethyl prostaglandin E2 (dm PGE2, 5 micrograms/kg) administered subcutaneously significantly increased duodenal mucosal alkaline secretion and significantly reduced the duodenal villous injury produced by 0.1 N HCl. The reduction in the severity of the lesion score was due to a decrease in the percentage of villi with the deeper type of damage. These data indicate: (1) perfusion of the rat duodenum with 0.1 N HCl at 0.1 ml/min for 30 min provides a valid model for assessing deep duodenal villous injury, (2) exogenous prostaglandin enhances the resistance of the duodenal mucosa against acid induced deep villous injury, and (3) the enhanced resistance may be mediated at least in part by stimulation of duodenal alkaline secretion. The results support the hypothesis that stimulated duodenal alkaline secretion may play a role in defense of the duodenal mucosa against acid-induced deep villous injury.

Animals↗

Absence of macrophage and presence of plasmacellular iron storage in the terminal duodenum of patients with hereditary haemochromatosis.

Biopsy specimens of the terminal duodenum obtained from 11 patients with hereditary haemochromatosis were examined by light and electron microscopy. Stainable iron was found in the lamina propria of the terminal duodenum in only 4 patients, all of whom were in an advanced stage of the disease. The iron was localized in the basal parts of the villi, sparing their tips, and between the crypts of Lieberkühn. The iron-storing cells could be identified as plasma cells, in which ferritin and haemosiderin were localized within lysosomes and ferritin molecules scattered in the cell sap. There was no storage of iron in macrophages. These observations demonstrate the impaired iron-storing capacity of macrophages in hereditary haemochromatosis, which may be related to the increased iron absorption in this iron storage disease.

Adult↗

Bradykinin action in the rat duodenum through the cyclic AMP system.

Activators of the adenylate cyclase or inhibitors of the cAMP-phosphodiesterase, respectively, potentiate the bradykinin-induced relaxation of the rat duodenum, whereas imidazole as a stimulator of the cAMP-phosphodiesterase reduces the relaxation. The experiments indicate a linkage between the adenylate cyclase system with the biological action of bradykinin on the rat duodenum. In contrast, no similar effect has been observed on the rat uterus.

3',5'-Cyclic-AMP Phosphodiesterases↗

Discordant effects of glucocorticoids on active and passive transport of calcium in the rat duodenum.

The effect of glucocorticoids on duodenal active and passive calcium transport was studied by the in situ intestinal loop technique, using 2.0 mM and 50 mM concentrations of calcium. The administration of prednisolone resulted in a significant increase of fluid and sodium absorption. The final luminal calcium concentration was increased in the prednisolone-treated group. Under conditions where active transport predominates (2 mM), glucocorticoids decreased lumen-to-plasma and increased plasma-to-lumen calcium flux, resulting in a decrease of net calcium absorption. Under conditions where passive transport predominates (50 mM), glucocorticoids did not decrease calcium absorption in the duodenum. These data suggest that under conditions where passive transport predominates, glucocorticoids indirectly enhance calcium absorption by an effect on water movement. Water movement enhances calcium absorption by concentrating unabsorbed calcium within the intestinal lumen. The increase in passive diffusion of calcium in the duodenum compensates for the inhibition of the active transport of calcium by glucocorticoids.

Animals↗

Blunt injury of duodenum with avulsion of papilla of Vater--report of a case.

In a 52-year-old man, there was a complete separation of the duodenum with avulsion of the papilla of Vater from the head of the pancreas due to blunt abdominal trauma. He was successfully treated by an anastomosis of the ampulla to the jejunum of a Roux-en Y limb, after removal of the entire duodenum and partial gastrectomy, followed by gastrojejunostomy of the Billroth II-type, instead of pancreaticoduodenectomy. The patient is well at 15 months after this surgery.

Ampulla of Vater↗

Synthesis and characterization of HPMC derivatives as novel duodenum-specific coating agents.

HPMC (Hydroxypropyl methylcellulose) was chemically modified, using maleic anhydrides, to obtain pH-sensitive HPMCAM (Hydroxypropyl methylcellulose acetate maleate) polymers for use as novel duodenum-specific coating agents. The pharmaceutical properties of HPMCAM, such as film forming, acid values, pH-sensitive values, water vapor permeability, tensile strength and Tg, were investigated, and found to show good film forming properties. The pH-sensitive values were 3.0 to 3.7. In vitro results demonstrate that HPMCAM could completely suppress drug release within 2h in a simulated gastric fluid (pH 1.2) and rapidly release the drug in a simulated pathological duodenal fluid (pH 3.4). These results indicate that HPMCAM might be a useful material for a duodenum-specific drug delivery system.

Berberine↗

Duodenum inversum mimicking mesenteric artery syndrome.

BACKGROUND: Duodenum inversum is an often unrecognized anomaly of duodenal rotation/fixation at upper gastrointestinal (UGI) contrast study because the duodenojejunal junction appears normally located. OBJECTIVE: This anomaly is important to diagnose because it may result in obstructive gastrointestinal symptoms. CONCLUSION: We describe a case of duodenum inversum mimicking superior mesenteric artery (SMA) syndrome that improved after surgical therapy.

Adolescent↗

T cell lymphoplasmacellular and eosinophilic infiltration of the pancreas with involvement of the gallbladder and duodenum in non-alcoholic duct-destructive chronic pancreatitis.

BACKGROUND: Non-alcoholic duct destructive chronic pancreatitis is a rare entity with specific pathological features. The majority of the patients are from Japan. We report a case with involvement of the distal bile duct, the gallbladder, the duodenum and the ampulla, and present a review of patients from Europe and the USA since 1997. CASE PRESENTATION: A 56-year-old man presented with a 3-month history of mild acute pancreatitis and obstructive jaundice, followed by increasing weight loss, lethargy and epigastric pain. CT showed a mass in the head of the pancreas. ERCP demonstrated a smooth stricture of the intra-pancreatic main bile duct and an irregular, incomplete, stricture in the main pancreatic duct. A pancreatic cancer could not be reliably excluded, and, therefore, he underwent a pylorus-preserving Kausch-Whipple's pancreatoduodenectomy. RESULTS: Histopathology showed typical peri-ductal T cell-rich lymphoplasmacellular and eosinophilic infiltration of the pancreas, with involvement of the distal bile duct but, also, unusual inflammatory infiltration of the gallbladder, the duodenum and the ampulla. CONCLUSION: The inflammatory process in non-alcoholic duct-destructive chronic pancreatitis can affect the entire pancreato-biliary region and mimics pancreatic cancer. Currently, there are no definitive criteria for pre-operative diagnosis, so it is very difficult for one to avoid resection.

Cholangiopancreatography, Endoscopic Retrograde↗

Pedicled ileal flap to repair large duodenal defect after right hemicolectomy for right colon cancer invading the duodenum.

Although right-sided colon cancer occasionally invades the second part of the duodenum, there is no standard procedure for reconstructing a large duodenal defect after resection. This report describes a new approach we recently devised. After resecting the right hemicolon and the involved duodenum, a segment of terminal ileum was isolated on the vascular pedicle, sacrificing the adjacent ileum. We created a flap by opening the segment along the antimesenteric border, and used this flap to cover the defect. This method does not create a nonanatomical bypass and fewer intestinal anastomoses are required than for Roux-en-Y reconstruction.

Aged↗