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PubMed1995

Impairment of nitrergic-mediated relaxation of rat isolated duodenum by experimental diabetes.

1. Diabetes mellitus is associated with changes in gastrointestinal motility. The effects of experimental diabetes, induced by streptozotocin administration to rats 3-4 weeks previously, on the nitric oxide (NO)-mediated (nitrergic) relaxation of the duodenum have now been investigated. 2. The non-adrenergic, non-cholinergic (NANC) relaxation of the isolated duodenum induced by nicotine (0.3-10 microM) or the nicotinic agonist, 1,1-dimethyl-4-phenylpiperazinium (DMPP; 10 microM) was inhibited by the NO synthase inhibitor, NG-nitro-L-arginine (3-100 microM). 3. This nitrergic relaxation induced by nicotine or DMPP of the duodenum from diabetic rats was substantially smaller than that of the tissue from control rats. 4. By contrast, the relaxation of the duodenum from diabetic rats to the NO donor, nitroprusside (0.3-10 microM) was similar to that of control tissue, whereas the relaxation to ATP (0.1-3 microM) was enhanced to a small but significant degree. 5. Incubation of duodenal tissue from control rats at 4 degrees C for 72 h, which leads to neuronal disruption, significantly attenuated the relaxation to nicotine or DMPP whereas the relaxation induced by nitroprusside or ATP was not affected. Comparable cold-storage did not affect the endothelium-dependent relaxation of rat aortic rings induced by acetylcholine (0.01-2 microM). 6. The calcium-dependent NO synthase activity in duodenal tissue, determined by the conversion of radiolabelled L-arginine to citrulline, was significantly reduced in cold-stored tissue and in tissue obtained from diabetic rats. 7. These findings in the rat duodenum indicate that a reduction in intestinal NO synthase activity is associated with an impairment of the NANC relaxation. A defect in the intestinal nitrergic innervation could thus contribute to the motility dysfunction observed in diabetes.

Adenosine Triphosphate↗

PubMed1995

Inhibitory action of PPADS on relaxant responses to adenine nucleotides or electrical field stimulation in guinea-pig taenia coli and rat duodenum.

1. The effect of pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) on the relaxant response to adenine nucleotides was examined in the carbachol-contracted guinea-pig taenia coli and rat duodenum, two tissues possessing P2y-purinoceptors. In addition, in the taenia coli PPADS was investigated for its effect on relaxations evoked by adenosine, noradrenaline and electrical field stimulation. In order to assess the selectivity of PPADS between P2-purinoceptor blockade and ectonucleotidase activity, its influence on ATP degradation was studied in guinea-pig taenia coli. 2. The resulting rank order of potency for the adenine nucleotides in guinea-pig taenia coli was: 2-methylthio ATP >> ATP > alpha,beta-methylene ATP with the respective pD2-values 7.96 +/- 0.08 (n = 23), 6.27 +/- 0.12 (n = 21) and 5.88 +/- 0.04 (n = 24). 3. In guinea-pig taenia coli, PPADS (10-100 microM) caused a consistent dextral shift of the concentration-response curve (CRC) of 2-methylthio ATP and ATP resulting in a biphasic Schild plot. A substantial shift was only observed at 100 microM PPADS, the respective pA2-values at this particular concentration were 5.26 +/- 0.16 (n = 5) and 5.15 +/- 0.13 (n = 6). Lower concentrations of PPADS (3-30 microM) antagonized the relaxant effects to alpha,beta-methylene ATP in a surmountable manner. An extensive shift of the CRC was produced only by 30 microM PPADS (pA2 = 5.97 +/- 0.08, n = 6), and the Schild plot was again biphasic. 4. The relaxant responses to electrical field stimulation (80 V, 0.3 ms, 5 s, 0.5-16 Hz) in guinea-pigtaenia coli were concentration-dependently inhibited by PPADS (10-100 microM).5. In guinea-pig taenia coli, the potency of ATP in inducing relaxation appeared to be independent of its rate of degradation by ecto-nucleotidases, since the Km-value (366 microM) obtained in the enzyme assay was much higher than the functional EC50-value (0.45 microM) of ATP. PPADS (3-100 microM) was only weakly active in inhibiting ecto-nucleotidase activity leaving a residual activity of 81.8 +/- 5.1% at 100 microM.Enzyme inhibition by PPADS was concentration-independent and non-competitive.6. In rat duodenum, the rank order of potency was: 2-methylthio ATP >ATP> >alpha,beta-methylene ATP,the respective pD2-values being 6.98 +/- 0.04 (n = 76), 6.26 +/- 0.02 (n = 6) and 4.83 +/- 0.02 (n = 6). Among these agonists, 2-methylthio ATP displayed the lowest apparent efficacy.7. The CRC of 2-methylthio ATP in rat duodenum was shifted to the right by PPADS (10-100 microM) ina concentration-dependent manner, and Schild analysis gave a pA2-value of 5.09 +/- 0.06 (slope = 1.02,n=14).8 PPADS was without any effect on the carbachol-induced contraction in guinea-pig taenia coli or rat duodenum and on the relaxation to noradrenaline or adenosine in guinea-pig taenia coli.9 In conclusion, the antagonistic properties of PPADS at the taenia coli and rat duodenum P2y-purinoceptors were different from those recently described at the P2x-subtype: inhibition of P2y-purinoceptor-mediated responses was observed at higher concentrations (3-100 microM vs. 1-10 (30) microM).Furthermore, we conclude that in addition to the classical P2y-subtype, which is largely PPADS-resistant,the guinea-pig taenia coli may be endowed with a distinct relaxation-mediating P2-purinoceptor subtype which is sensitive to PPADS.

Adenosine↗

PubMed1996

Characterization of P1-purinoceptors on rat isolated duodenum longitudinal muscle and muscularis mucosae.

1. P1-purinoceptors mediating relaxation of the rat duodenum longitudinal muscle and contraction of the rat duodenum muscularis mucosae were characterized by the use of adenosine and its analogues, 5'-N-ethylcarboxamidoadenosine (NECA), N6-cyclopentyl-adenosine (CPA), N6-(phenylisopropyl)adenosine (R-PIA), 2-chloroadenosine (2-CADO) and 2-p-((carboxyethyl)phenethylamino)-5'-carboxamidoadenosine (CGS21680), as well as the P1-purinoceptor antagonist 8-phenyltheophylline (8-PT) and the A1-selective antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). 2. In the rat duodenum longitudinal muscle, the order of potency of the adenosine agonists was CPA > NECA > adenosine > CGS21680. DPCPX antagonized responses to CPA and NECA at a concentration of 1 nM suggesting that they are acting at A1 receptors. A Schild plot versus CPA gave a slope near to unity (slope = 0.955) and a pA2 of 9.8 confirming that CPA was acting via A1 receptors. Schild analysis for DPCPX versus NECA, however, gave a slope of 0.674 suggesting that NECA was acting on both A1 and A2 receptors. CGS21680, a selective A2a agonist, was much less potent than adenosine suggesting that the A2 receptors are of the A2b subtype. 3. In the rat duodenum muscularis mucosae, the order of potency of the adenosine agonists was NECA > or = R-PIA = CPA > 2-CADO > adenosine, and DPCPX antagonized responses to CPA and NECA at a concentration of 1 microM. CGS21680, at a concentration of 10 microM, had no effect on this tissue. This suggests the presence of A2 receptors in this tissue and that they are of the A2b subtype. 4. These results are in agreement with previous studies in the whole duodenum showing the presence of A1 and A2b receptors causing relaxation, and this shows that the longitudinal muscle dominates the response of the whole tissue. In addition, a contractile A2b receptor has been revealed on the muscularis mucosae, the first time this subtype has been reported to elicit an excitatory response in a smooth muscle preparation.

Adenosine↗

PubMed1982

The effect of antrectomy on the number of gastrin-immunoreactive cells in the canine duodenum.

The number of gastrin-immunoreactive cells in the duodenum was assessed by immunohistochemistry in 10 dogs that had been subjected to antrectomy with gastroduodenostomy (Billroth I), in 4 dogs in which an antrectomy with gastrojejunostomy (Billroth II) had been performed and in 4 unoperated controls. Gastrin-immunoreactive cells were found only in dogs that had been subjected to antrectomy ad modum Billroth I and then only within the first 30 mm of the duodenum, i.e. in the duodenal bulb. The gastrin cells occurred scattered on the villi, in the crypts and within the glands of Brunner. In 3 of the dogs patches of antral-type mucosa occurred within the first 10 mm of the duodenum. All dogs in which gastrin-immunoreactive cells were found have in a previous study been shown to have a markedly increased tissue concentration of gastrin in the proximal third of the duodenum compared to unoperated controls. In the dogs subjected to antrectomy ad modum Billroth II in which no cells were observed the level of gastrin in duodenal tissue has been found to be moderately elevated compared to that of control dogs. The results indicate that the increased gastrin concentration in the proximal third of the duodenum following antrectomy ad modum Billroth I corresponds to an increase in the number of gastrin-immunoreactive cells in the duodenal bulb.

Animals↗

PubMed1981

Secretin release from the isolated, vascularly perfused pig duodenum.

1. A method for the isolation and vascular perfusion of the porcine pancreas and duodenum was developed. 2. The oxygen consumption of the whole preparation was similar to that of the pancreas alone, and since the duodenal arteriovenous oxygen deficit was similar to that of the total preparation, it was concluded that the duodenum respired adequately. 3. The duodenum rapidly absorbed luminally administered radioactive glucose, and this absorption was strongly inhibited by ouabain and phloridzin. 4. The duodenum secreted secretin rapidly in response to hydrochloric acid, but did not respond to any other luminal stimuli, including lipids, proteins, carbohydrates and bile. Neither was secretin release stimulated by intra-arterially injected acetylcholine. 5. By gel permeation chromatography the release immunoreactive secretin behaved identically to pure natural secretin, indicating that the tissue form and the circulating form have identical molecular size. 6. It is concluded that this model offers an unique opportunity to study the endocrine secretion of the duodenum.

Animals↗

PubMed1995

Tyrosine phosphorylation in the human duodenum.

Many growth factor receptors including the epidermal growth factor receptor function through tyrosine kinase activity. The aim of this study was to examine the constitutive level of tyrosine phosphorylation in the normal duodenum and in the hyperproliferative coeliac duodenum. A flow cytometric assay was devised using monoclonal antibody to phosphorylated (but not native) tyrosine residues to determine the levels of tyrosine phosphorylation in both CD3 positive intraepithelial lymphocytes and CD3 negative epithelial cells obtained by EDTA treatment of endoscopically obtained duodenal biopsy specimens. In addition, immunohistochemistry was performed on 18 formalin fixed coeliac duodenal biopsy specimens and eight control specimens. Tyrosine phosphorylation could be detected by flow cytometry on duodenal enterocytes and this expression was up regulated by pretreatment with epidermal growth factor. Tyrosine phosphorylation decreased with progression from the villus to the crypt, however, and was virtually undetectable on crypt enterocytes. Immunohistochemistry of the coeliac duodenum showed virtually absent tyrosine phosphorylation in the crypt. Increased tyrosine phosphorylation was detected in the infiltrating T cells. In conclusion, tyrosine phosphorylation in the duodenum is confined to the non-proliferative villous epithelium and is virtually undetectable in the proliferative crypt compartment. These findings suggest that tyrosine kinase activity is not a significant factor in the regulation of crypt cell proliferation in the human duodenum either in normal subjects or in coeliac disease patients.

CD3 Complex↗

PubMed1996

Circadian gastric acidity in Helicobacter pylori positive ulcer patients with and without gastric metaplasia in the duodenum.

BACKGROUND: The presence of gastric metaplasia allows helicobacter pylori to colonise the duodenum and this condition is thought to be acquired as a response to acid hypersecretion. This functional disorder, however, is present only in a subgroup of duodenal ulcer patients and, in addition, surface gastric metaplasia has been frequently found in the proximal duodenum of normal subjects and patients with non-ulcer dyspepsia, who cannot be certainly considered as acid hypersecretors. AIMS: To clarify the role of acid in inducing gastric type epithelium in the duodenum. This study aimed at assessing whether the pattern of circadian gastric acidity differs between H pylori positive duodenal ulcer patients with and without duodenal gastric metaplasia. PATIENTS: Seventy one patients with duodenal ulcer confirmed by endoscopy and who were found to be positive for H pylori infection by histology on antrum biopsy specimens were enrolled into this study. METHODS: Gastric type epithelium in the duodenum was found in 49 of 71 ulcer patients (69%). Continuous 24 hour gastric pH metry was performed in 50 healthy subjects and in the two subgroups of duodenal ulcer patients with and without gastric metaplasia in the duodenum. Gastric acidity was calculated for 24 hours (1700-1659), night (2000-0759) and day-time (0800-1959). RESULTS: Ulcer patients without gastric metaplasia showed a significantly higher gastric acidity (p < 0.001) than controls for every time interval considered, while the ulcer subgroup with gastric metaplasia was more acid than healthy subjects (p < 0.001) during the whole 24 hour period and the daytime. There was no difference between the two subgroups of duodenal ulcer patients with and without gastric metaplasia during the various time segments analysed. CONCLUSION: The findings confirm that the circadian gastric acidity of duodenal ulcer patients is higher than that of controls. As there is no difference in gastric pH between duodenal ulcer patients with and without gastric metaplasia, gastric hyperacidity is not specific to patients with duodenal gastric metaplasia. It is probable that this histological change is a non-specific response to mucosal injury resulting from various factors and not exclusively to acid.

Adult↗

PubMed1982

Surface epithelial HCO3(-) transport by mammalian duodenum in vivo.

Duodenal surface epithelial transport of HCO3(-) was measured by direct titration in anesthetized animals. Alkalinization of the lumen occurred in all species, although basal rates varied considerably: rats (approximately 10), cats (approximately 15), pigs (approximately 25), dogs (approximately 25), guinea pigs (approximately 40), and rabbits (approximately 170 mueq.cm-1.h-1). In cats duodenum transported HCO3(-) at a greater basal rate than jejunum (approximately 5 mueq.cm-2.h-1) and developed a higher transmucosal electrical potential difference (PD, lumen negative). Luminal application of 10 mM HCl for 5 min produced a sustained increase in the rate of duodenal HCO3(-) transport that was accompanied by a rise in appearance of E-like prostaglandin immunoreactivity in the lumen and a decrease in DNA release. In cats pretreated with indomethacin (10 mg/kg iv), acid caused only a transient increase in HCO3(-) transport. Exogenous prostaglandin E2 (1-12 microM, luminal) increased basal HCO3(-) transport in cats, rats, and dogs but had no effect on this transport in guinea pigs and rabbits. However, prostaglandin E2 increased HCO3(-) transport and PD in guinea pigs pretreated with inhibitors of tissue cyclooxygenase activity (indomethacin or aspirin) or gastric H+ secretion (cimetidine). Thus the continuous exposure of the duodenum of herbivores to HCl discharged from the stomach may itself stimulate HCO3(-) transport via an increase in endogenous prostaglandin levels and render exogenous prostaglandins ineffective. Secretin (1-15 CU/kg iv) was without effect in both cats and guinea pigs. In guinea pigs, intravenous glucagon (120-360 micrograms.kg-1.h-1) or gastric inhibitory peptide (5 micrograms/kg) both increased HCO3(-) transport but not PD. Hence, prostaglandin-stimulated and hormone-stimulated mechanisms of HCO3(-) transport probably occur in mammalian duodenum as found previously in the isolated amphibian duodenum. The results suggest that epithelial HCO3(-) transport is a major mechanism of acid disposal, and thus mucosal protection, in mammalian duodenum under the control of hormones and endogenous prostaglandins.

Animals↗

PubMed1983

Measurement of cholecystokinin octapeptide-induced motility of rat antrum, pylorus, and duodenum in vitro.

Motor effects of cholecystokinin octapeptide (CCK-OP) on rat antrum, pylorus, and duodenum have been studied in vitro under standard conditions. Intraluminal pressure changes were simultaneously measured at the three locations using a perfusion manometric system with a novel intraluminal pressure-sensor device. This device comprised an acrylic cast of the rat gastroduodenal tract containing the perfusion catheters that reached the surface of the cast with their outlets in the antrum, pylorus, and duodenum. A selective and sensitive intraluminal local pressure measurement was achieved with this pressure sensor due to its shape. CCK-OP increased base-line pressure in the antrum, pylorus, and duodenum; frequencies of phasic contractions in the antrum and pylorus; and amplitudes in the duodenum. The peptide also decreased contraction amplitudes in the antrum and pylorus and frequency of phasic contractions in the duodenum. It is concluded that the novel intraluminal pressure sensor is a useful tool for measuring local pressure changes in the gastroduodenal tract of the rat. In this experimental model, effects of CCK-OP on antral, pyloric, and duodenal base-line pressure are comparable with those observed in isolated muscle strips and in the intact organ of humans, dogs, and opossums. A different behavior, however, was observed in the force of antral and frequency of duodenal phasic contractions.

Animals↗

PubMed1998

Dual role of CFTR in cAMP-stimulated HCO3- secretion across murine duodenum.

The role of the cystic fibrosis transmembrane conductance regulator (CFTR) in cAMP-stimulated HCO3- secretion across the murine duodenum was investigated. Serosal-to-mucosal flux of HCO3- (Js-->m, in mu eq.cm-2.h-1) and short-circuit current (Isc; in mu eq.cm-2.h-1) were measured by the pH stat method in duodenum from CFTR knockout [CFTR(-)] and normal [CFTR(+)] mice. Under control conditions, forskolin increased Js-->m and Isc (+1.7 and +3.5, respectively) across the CFTR(+) but not CFTR(-) duodenum. Both the forskolin-stimulated delta Js-->m and delta Isc were abolished by the CFTR channel blocker 5-nitro-2-(3-phenylpropylamino)benzoate, whereas inhibition of luminal Cl-/HCO3- exchange by luminal Cl- removal or DIDS reduced the Js-->m by approximately 18% without a consistent effect on the delta Isc. Methazolamide also reduced the Js-->m by 39% but did not affect the delta Isc. When carbonic anhydrase-dependent HCO3- secretion was isolated by using a CO2-gassed, HCO3(-)-free Ringer bath, forskolin stimulated the Js-->m and Isc (+0.7 and +2.0, respectively) across CFTR(+) but not CFTR(-) duodenum. Under these conditions, luminal Cl- substitution or DIDS abolished the Js-->m but not the delta Isc. It was concluded that cAMP-stimulated HCO3- secretion across the duodenum involves 1) electrogenic secretion via a CFTR HCO3- conductance and 2) electroneutral secretion via a CFTR-dependent Cl-/HCO3- exchange process that is closely associated with the carbonic anhydrase activity of the epithelium.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed2005

Leptin and CCK selectively activate vagal afferent neurons innervating the stomach and duodenum.

The hormone leptin and the gut peptide CCK synergistically interact to enhance the process of satiation. Although this interaction may occur at several levels of the neuroaxis, our previous results indicate that leptin can specifically enhance the satiation effect of CCK by acting on subdiaphragmatic vagal afferent neurons. Because of this localized action, we hypothesized that a high proportion of vagal afferent neurons innervating the stomach or duodenum would be responsive to leptin and/or CCK. To test this hypothesis, we measured changes in cytosolic calcium levels induced by leptin and CCK in cultured nodose ganglion neurons labeled with a retrograde neuronal tracer injected into either the stomach or the duodenum. In the neurons labeled from the stomach, CCK activated 74% (39 of 53) compared with only 35% (34 of 97) of nonlabeled cells. Of the CCK-responsive neurons 60% (18 of 30) were capsaicin-sensitive. Leptin activated 42% (22 of 53) of the stomach innervating neurons compared with 26% of nonlabeled neurons. All of the leptin-sensitive neurons labeled from the stomach also responded to CCK. In the neurons labeled from the duodenum, CCK activated 71% (20 of 28). Of these CCK-responsive neurons 80% (12 of 15) were capsaicin sensitive. Leptin activated 46% (13 of 28) of these duodenal innervating neurons, of which 89% (8 of 9) were capsaicin-sensitive. Among neurons labeled from the duodenum 43% (12 of 28) were responsive to both leptin and CCK, compared with only 15% (15 of 97) of unlabeled neurons. Our results support the hypothesis that vagal afferent sensitivity to CCK and leptin is concentrated in neurons that innervate the stomach and duodenum. These specific visceral afferent populations are likely to comprise a substrate through which acute leptin/CCK interactions enhance satiation.

Animals↗

PubMed1990

Relationship between fluctuations of pH and pressure in the human stomach and duodenum.

The normal patterns of pressure activity in the antrum, pylorus and duodenum and associated pH changes were monitored in 9 healthy volunteers under fasted conditions and after ingestion of 300 ml of chocolate milk. The manometric assembly incorporated three side holes in the antrum, four side holes in the duodenum, a sleeve sensor positioned across the pylorus, and pH electrodes situated in the terminal antrum and proximal duodenum. The most common motor pattern recorded under fasting conditions consisted of regular co-ordinated contractions, most of which involved the antrum and duodenum, showed evidence of propagation and was associated with transient decreases in duodenal pH and transient increases in antral pH. Ingestion of milk changes the motor pattern to one that was composed of pressure waves which were confined to the pylorus with few or no pressure waves in the terminal antrum or proximal duodenum. Isolated pyloric pressure waves were gradually replaced by propagated antropyloroduodenal contractions which were associated with transient decreases in duodenal pH. Isolated pyloric pressure waves were not associated with episodes of duodenal acidification under fed conditions.

Adult↗

PubMed2006

A prospective study of differences in duodenum compared to remaining small bowel motion between radiation treatments: implications for radiation dose escalation in carcinoma of the pancreas.

PURPOSE: As a foundation for a dose escalation trial, we sought to characterize duodenal and non-duodenal small bowel organ motion between fractions of pancreatic radiation therapy. PATIENTS AND METHODS: Nine patients (4 women, 5 men) undergoing radiation therapy were enrolled in this prospective study. The patients had up to four weekly CT scans performed during their course of radiation therapy. Pancreas, duodenum and non-duodenal small bowel were then contoured for each CT scan. On the initial scan, a four-field plan was generated to fully cover the pancreas. This plan was registered to each subsequent CT scan. Dose-volume histogram (DVH) analyses were performed for the duodenum, non-duodenal small bowel, large bowel, and pancreas. RESULTS: With significant individual variation, the volume of duodenum receiving at least 80% of the prescribed dose was consistently greater than the remaining small bowel. In the patient with the largest inter-fraction variation, the fractional volume of non-duodenal small bowel irradiated to at least the 80% isodose line ranged from 1% to 20%. In the patient with the largest inter-fraction variation, the fractional volume of duodenum irradiated to at least the 80% isodose line ranged from 30% to 100%. CONCLUSION: The volume of small bowel irradiated during four-field pancreatic radiation therapy changes substantially between fractions. This suggests dose escalation may be possible. However, dose limits to the duodenum should be stricter than for other segments of small bowel.

Dose-Response Relationship, Radiation↗

PubMed1979

[Decrease of ACh response in isolated duodenum from SART stressed (repeated cold stressed) mice (author's transl)].

ACh response in the isolated duodenum from SART stressed (repeated cold stressed) mice was remarkably decreased in comparison to normal mice 5 days after onset of loading SART stress, and maximal contraction in SART stress mice duodenum was about 37% of that in non-stressed mice. Pilocarpine and KCl responses were also considerably decreased, but BaCl2 response was much the same as in the controls. Thus, the contraction system of the muscle is apparently not damaged by SART stress. Though body weights decreased, the daily intake of food incressed in SART stressed mice. Length of small intestine from SART stressed mice was much the same as in controls, but wet weights of small intestines were larger than in controls. Autonomic agonists, antagonists, tranquilizers and other drugs were given intraperitoneally to mice once daily during SART stress, and the ACh responses in the isolated duodenum were investigated. Pretreatment with adrenergic and anticholinergic drugs inhibited the decrease of ACh response, but antiadrenergic and cholinergic drugs had no effects. Pretreatment with tranquilizers such as reserpine, chlorpromazine, carpipramine and imipramine inhibited the decrease of ACh response in the isolated duodenum, but diazepam, meprobamate and benadryl had no influence. Pretreatment of neurotropin, a neurosedative had good inhibitory effects. Our results suggest that SART stressed mice may be in a state of unbalance regarding sympathetic and parasympathetic nerves, particularly with regard to abnormal tension in the parasympathetic nervous system, in part of duodenum. Pretreatment with most of the above drugs had no influence on loss of body weight in SART stressed mice while pretreatment with neurotropin inhibited body weight to a considerable extent.

Acetylcholine↗

PubMed1978

Site of emetic action of oral copper sulfate in dogs. (II) Importance of lower duodenum.

Sensitivities of the stomach and duodenum to oral copper sulfate emesis were compared in dogs. 1) Dogs equipped with a stainless stell cannula in the middle of the duodenum were challenged to the oral threshold emetic dose of copper sulfate administered by a gastric tube. When the cannulas were opened, the oral thresholds were not effective to elicit vomiting in the most cases (1/13). Fairly rapid and high rate recoveries of copper through the open cannula were noted. With the closed cannulas, the thresholds were highly effective (16/16). 2)In the dogs with a cannula at the upper part of the jejunum, the oral threshold doses were always effective whether the canula was opened (9/9) or closed (11/11). Recovery rates of copper from the cannula were usually poor. 3) The oral thresholds administered into the proximal end or the middle of the duodenum through a PVC tubing were equally effective. 4) Although copper sulfate might irritate the stomach and upper duodenum to evoke vomiting, these results suggested a higher sensitivity of the lower duodenum.

Administration, Oral↗

PubMed1988

[Effects of cholecystokinin-octapeptide and tetragastrin on the contractile activities of the stomach, duodenum and papilla of Vater].

Effects of cholecystokinin-octapeptide (CCK-OP) and tetragastrin (TG) on the stomach, duodenum and papilla of Vater were examined using 13 adult dogs. The contractile activities of the stomach and duodenum were examined using the strain gage, and the manometric study of the papilla of Vater was also performed. CCK-OP increased the contractile activities of the stomach and duodenum, but at the same time the pressure of the papilla of Vater was decreased. TG increased the contractile activities of the stomach, but decreased that of the duodenum and the pressure of papilla of Vater. CCK-OP lowered the pressure of the common bile duct, and that fall corresponded with the disappearance of the phasic contraction of the papilla of Vater. We concluded that the contractile activity of the papilla of Vater was independent of the contractile activity of the duodenum, and the most effective drainage of the bile was achieved at the time of the disappearance of the phasic contraction of the papilla of Vater.

Ampulla of Vater↗

PubMed1990

Fat inhibits pentagastrin-stimulated acid secretion from the duodenum but not from the proximal jejunum in chronic gastric fistula rats.

The effect of fat emulsion in the upper intestine on the maximal gastric acid response to pentagastrin was studied in chronic gastric fistula (GF) rats with a 4-cm blind loop of the duodenum anastomosed to the jejunum (Roux-en-Y). Fat emulsion in the loop inhibited the acid response by 85%. To localize the site of the inhibitory mechanism, GF rats were provided with Thirty-Vella loops of the duodenum (bile and pancreatic ducts transplanted to the proximal jejunum) or with Thirty-Vella loops of the proximal jejunum and a Roux-en-Y loop of the duodenum to prevent gastric juice from entering the duodenum. Perfusion of the duodenal loop with fat emulsion mixed with bile and pancreatic juice reduced the acid response by 49%, but perfusion of the proximal jejunal loop did not alter the response. It is concluded that the intestinal mechanism for inhibition of acid secretion by fat is located in the duodenum in rats.

Anastomosis, Roux-en-Y↗

PubMed1997

Electrogenic ion transport along the human duodenum in childhood.

BACKGROUND: To find reliable sites to study the effects of different secretagogues on electrogenic ion secretion, we investigated the secretion pattern in different parts of duodenum. METHODS: Histologically normal routine intestinal biopsy specimens from children were mounted in a modified Ussing chamber. The secretory responses to prostaglandin E2 (PGE2), aminophylline, dibutyryl cyclic adenosine 5'-monophosphate (cAMP), and acetylcholine (ACh) were studied with continuous measurements of the potential difference. Tissue resistance and generated current were calculated. RESULTS: ACh induced secretion in the whole of duodenum, although the secretory response was augmented distally. PGE2 and cAMP induced significant secretion only in the distal duodenum. CONCLUSIONS: The ACh-induced, calcium-mediated, electrogenic secretion was expressed along the whole duodenum, whereas the cAMP-mediated secretion was only seen in the distal part. The fully expressed electrogenic chloride secretion was only seen at or distal to the duodenojejunal flexure. Our study shows that it is important to carefully define the localization of physiologic studies performed in the duodenum.

Acetylcholine↗