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PubMed1985

Bile duct obstruction by villous papilloma of duodenum.

Two cases of peri-ampullary villous adenomas involving the common bile duct are reported. The pathology of benign duodenal tumours is discussed, and the possibility of common bile duct involvement, albeit uncommon, is stressed. Obtaining an endoscopic histologic diagnosis is important in planning appropriate operative treatment. Although benign, these tumours should be removed; they are a cause of serious symptoms and have proven premalignant potential. Endoscopic removal is usually not possible. Endoscopy for dyspepsia should include examination of the second part of duodenum, to avoid overlooking duodenal tumours.

Aged↗
PubMed1995

Nitric oxide is involved in non-adrenergic, non-cholinergic inhibitory neurotransmission in rat duodenum.

1. In rat duodenum, electrical field stimulation (EFS) induced a relaxation due to activation of non-adrenergic, non-cholinergic (NANC) inhibitory intramural neurones. 2. Nitric oxide synthase (NOS) inhibitors, N omega-nitro-L-arginine (L-NNA) and N omega-nitro-L-arginine methyl ester (L-NAME), caused a dose-dependent reduction in amplitude of the NANC relaxation. Responses to low frequencies of stimulation were more sensitive to NOS inhibitors than those to high frequencies. 3. Effects induced by NOS inhibitors were stereospecific since D-NNA and D-NAME did not affect NANC relaxation. L-arginine, but not D-arginine, partially prevented the effects induced by NOS inhibitors on NANC relaxation. 4. The nitrovasodilator drug, sodium nitroprusside, caused muscle relaxation which was not affected by preincubation with either tetrodotoxin (TTX), L-NNA or L-NAME. 5. alpha-Chymotrypsin reduced relaxations elicited by stimulation of NANC nerves, especially when high frequencies of stimulation were used. The residual NANC relaxation was further reduced by NOS inhibitors. In the same way, alpha-chymotrypsin was able to further reduce the relaxation observed after NOS inhibitors. 6. These results suggest that nitric oxide (NO) and a peptide are involved in NANC relaxation of rat duodenal smooth muscle. NO and peptidergic pathways act in parallel to produce muscle relaxation and they are preferentially activated by stimuli at low and high frequencies, respectively.

Amino Acid Oxidoreductases↗
PubMed1973

Nerve-mediated inhibition of mechanical activity in rabbit duodenum and the effects of desensitization to adenosine and several of its derivatives.

1. Inhibition of mechanical activity in longitudinal muscle strips of rabbit duodenum was induced by perivascular and intramural nerve stimulation.2. The effects of perivascular stimulation were abolished by phentolamine + propranolol, guanethidine, reserpine and by tetrodotoxin. The effects of intramural stimulation were abolished only by tetrodotoxin.3. Noradrenaline, phenylephrine, isoprenaline, adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and adenosine each produced an inhibition of mechanical activity. The relative potencies of these agonists were noradrenaline>isoprenaline>phenylephrine>ATP>ADP>adenosine>AMP.4. Exposure of tissues to high concentrations of either ATP or adenosine desensitized the tissue to further exposure to ATP, ADP, AMP and adenosine, whilst the inhibitory effects of noradrenaline, phenylephrine and isoprenaline and of perivascular and intramural stimulation were unaffected. The effects of desensitization were reversible.5. It was concluded that the effects of intramural stimulation were mediated neither by noradrenaline nor by adenosine or its derivatives.

Adenosine↗
PubMed1979

Characterization of ultraviolet light-induced relaxation of the isolated duodenum of the rat.

1 Isolated duodenum of the rat, exposed to ultraviolet (u.v.) light in the presence of NO2 ions, responded with reversible relaxation. 2 The photorelaxation response did not seem to involve any known receptor mechanisms and was independent of any ganglionic or neuronal influences. 3 Changes in the ionic environment of the tissue showed that NA+ and Ca2+ were essential for the photorelaxation. K+ depolarized-tissue did not show the photoresponse. 4 The presence of the metabolic inhibitors, iodoacetic acid, 2,4-dinitrophenol, sodium fluoride, sodium azide or potassium cyanide, abolished the photorelaxation response. 5 It is proposed that the photorelaxation of the tissue resulted from the liberation of metabolic energy following NO2 ion-dependent absorption of u.v. light energy, which in turn, interfered with the Na+ ion movement across the cell membrane.

Animals↗
PubMed1984

Potassium induces relaxation and hyperpolarization of circular muscles but contraction of longitudinal muscles of pig duodenum.

The mechanisms by which K+ relaxes circular muscles of pig duodenum were investigated, and compared with the response of the longitudinal muscles to K+. Circular muscles were concentration-dependently relaxed by 8.3-23.6 mM K+, but contracted by 47.2-143.4 mM K+. Longitudinal muscles were contracted by 11.8-94.4 mM K+. The relaxation of circular muscles was correlated with hyperpolarization (4 mV), but evoked Ca2+ spikes were not suppressed. Neither ouabain (0.14 microM) nor phentolamine (10 microM) blocked the relaxation, but tetrodotoxin (TTX, 0.63 microM) blocked both the relaxation and hyperpolarization. Mesaconitine (0.16 microM) increased the relaxation. Inhibitory junction potentials and concomitant relaxations were also blocked by TTX. The results suggest that K+-induced relaxation is caused by the release of a non-adrenergic inhibitory transmitter.

Animals↗
PubMed1993

The Leu13-motilin (KW-5139)-evoked release of acetylcholine from enteric neurones in the rabbit duodenum.

1. Involvement of cholinergic mechanisms in the contractile response to Leu13-motilin (LMT, KW-5139) was investigated in rabbit duodenal segments, and longitudinal muscle-myenteric plexus (LM-MP) preparations preincubated wtih [3H]-choline. 2. Contractile response to LMT (0.1 nM-1 microM) consisted of an initial rapid (phasic) contraction and a tonic contraction slowly fading to a sustained plateau. LMT caused a concentration-dependent phasic contraction of rabbit isolated duodenal segments. The EC50 value was 2.5 nM and the maximum amplitude of the contraction was 103% of the response induced by acetylcholine (ACh, 100 microM). Neither tetrodotoxin nor atropine changed the EC50 value or the maximum amplitude of the response to LMT. 3. Both atropine and tetrodotoxin decreased the amplitude and accelerated fading of the tonic contraction produced by LMT. 4. LMT (30 nM-3 microM) induced an increase of 3H-outflow, in a concentration-dependent manner. The LMT-induced increase of 3H-outflow was prevented by removal of external Ca2+ or by the presence of tetrodotoxin. 5. Porcine motilin (10 nM-1 microM) also stimulated the release of 3H at a similar concentration-range to that seen with LMT. 6. Pretreatment with LMT (3 microM for 20 min) decreased LMT- and the porcine motilin-evoked release of 3H but did not alter the high K(+)-evoked release. 7. Our results suggest that LMT and porcine motilin stimulate the release of ACh from enteric neurones through the same receptor, and that the release of ACh plays a role in tonic components of contraction in the rabbit duodenum.

Acetylcholine↗
PubMed1999

Primary biliary cystadenocarcinoma perforating the duodenum and left intrahepatic biliary tree--mimicking a hydatid cyst.

We report the case of a 76-year-old woman with biliary cystadenocarcinoma perforating the left biliary tree and exhibiting intra-tumoral gas bubbles resulting from invasion of the duodenum. The clinical history included subfebrile temperatures of 3 months duration, and pains associated with an abdominal mass in the right upper quadrant. Blood tests showed leucocytosis, and radiological studies revealed the features of a partially calcified septated tumor with nodular components combined with multiple gas-fluid levels, mimicking an infected hydatid cyst. Intraoperative ultrasonography, cholangiography and frozen section histology were necessary to prove the malignant nature of this cystic tumor. Provided that complete resection with strict adherence to oncological precepts is possible, the prognosis of cystadenocarcinoma is better than in hepatocellular or cholangiocellular carcinoma.

Aged↗
PubMed1991

Atipamezole, benzodiazepines, bicucullin and tifluadom antagonize the effect of TRH on rat duodenum and displace it from brain and anterior pituitary receptors.

The mechanism of action of the TRH induced inhibition of contractions of the transmurally stimulated rat duodenum has been studied. The effect of TRH was not antagonized by atropine, pentolinium, phenoxybenzamine, sotalol, methysergide, domperidone, diphenhydramine, cimetidine, aminophylline, antazolin, indomethacin, morphine, naloxone or tetrodotoxin. In contrast, the adrenergic alpha 2-antagonist atipamezole, the benzodiazepines chlordiaxepoxide and midazolam or GABA-A-antagonist bicucullin but not picrotoxin or SR-95531 attenuated the response to TRH. An opioid-kappa-receptor agonist having benzodiazepine structure, tifluadom, but not MR 2034 also diminished the response to TRH. However, these actions were not modified by the alpha 2-agonist medetomidine, benzodiazepine antagonist flumazenil, GABA-agonists muscimol or baclofen or naloxone, respectively. While the binding of [3H][3-Me-His2]TRH to the rat anterior pituitary, hypothalamus, cortex and brainstem homogenates was saturable and of high affinity, no saturable binding was observed in the duodenal smooth muscle. Agents that were effective in the duodenal preparation displaced [3H][3-Me-His2]TRH from its binding sites in brain homogenates and the inhibitory constants (Ki) were (in microM): 0.038-0.107 (TRH), 0.19-5.8 (chlordiazepoxide), 0.021-8.9 (midazolam), 1.5-17 (tifluadom), 60-210 (bicucullin) and 150-530 (atipamezole). Atipamezole, bicucullin and chlordiazepoxide caused competitive displacement indicated by the increased KD of the labelled ligand but no change in the Bmax while tifluadom increased KD and decreased Bmax. It is concluded that the inhibitory effect of TRH on the contractions of the duodenal smooth muscle is mediated directly by the smooth muscle and it is apparently specific for TRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Modification of the gastric secretory response to sham feeding by acidification of the antrum and the duodenum in dogs.

The effect of closure of a gastric cannula on the acid response to sham feeding was studied in Pavlov-pouch dogs with intact antro-duodenal regions as well as in antrectomized dogs with gastroduodenostomies. In the latter dogs, the sham feeding response was augmented by infusions of low doses of exogenous gastrin. The acid output after sham feeding in intact dogs was reduced on average by 59% by closure of the gastric cannula. In antrectomized dogs receiving a back-ground stimulation with gastrin, the response to ham feeding was not inhibited by closure of the cannula. The results suggest that the observed hypersecretory response to sham feeding after diversion of gastric acid from antrum and duodenum is mainly due to inactivation of antral inhibitory mechanisms. The pepsin secretion following sham feeding was not consistently changed by closure of the gastric cannula.

Animals↗
PubMed1983

Molecular forms of gastrin in canine duodenum after antrectomy.

Extracts of the proximal third of the duodenum from 8 antrectomized dogs with the gastrointestinal continuity restored by gastroduodenostomy (n = 4) or gastrojejunostomy (n = 4) as well as from 4 unoperated controls were subjected to gel chromatography. The eluates were all assayed using two different gastrin antisera, one directed against the COOH-terminal end of gastrin and the other directed against the NH2-terminal end of gastrin-17. The gastrin component pattern was very similar in all antrectomized dogs regardless if they had a gastroduodenostomy or a gastrojejunostomy. Gastrin-17 was found to dominate while the amount of gastrin-34 was at most one tenth of that of gastrin-17. Using the COOH-terminal directed antiserum approximately 15% (mean value) of the total gastrin-like immunoreactivity eluted in a peak appearing in the same region as the COOH-terminal octapeptide of cholecystokinin. In unoperated control dogs the corresponding peak constituted approximately 70% (mean value) of the total gastrin-like immunoreactivity. In two of the control dogs small amounts of gastrin-like immunoreactivity appeared at the elution volumes of gastrin-34 and gastrin-17. In the duodenal extracts of all dogs gastrin-like immunoreactivity was found between the elution sites of gastrin-34 and gastrin-17. This material probably represents cholecystokinin-33. The present results show that the increase in duodenal gastrin found after antrectomy, which we have reported previously, is due mainly to an increase in gastrin-17.

Animals↗
PubMed1984

Stimulation of mucosal bicarbonate secretion in rat duodenum in vivo by BW755C.

Bicarbonate secretion from 12 mm segments of duodenum just distal to the Brunner's gland area was titrated (pH 7.60) in situ in anesthetized rats. Intravenous BW755C (10-20 mg/kg) increased both bicarbonate secretion and the transmucosal electrical potential difference and pretreatment with indomethacin (3 mg/kg intravenously) prevented these effects. Indomethacin also inhibited stimulation of HCO3- secretion by luminal acid (10 mM HCl) but had no effect on the rise in secretion in response to exogenous (luminal) prostaglandin E2. The results support previous suggestions of a role for endogenous prostaglandins in mediation of the HCO3- response to acid and are consistent with the recent demonstration that BW755C increased prostaglandin formation in homogenates of rat intestinal mucosa. Stimulation of HCO3- secretion by BW755C was not enhanced but attenuated by preexposure to luminal acid, suggesting that the latter increases secretion by effects other than mucosal mobilization of arachidonate.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1987

Effect of neuroactive agents on cholecystokinin release from the isolated, perfused porcine duodenum.

To elucidate the mechanisms involved in the regulation of CCK release from the small intestine, the effect of neuroactive agents on the release of CCK from the isolated, perfused porcine duodenum has been studied. CCK in the venous effluent was measured by three radio-immunoassays specific for the N-terminus, the tyrosine-o-sulphated region and the C-terminus of CCK-33. Gastrin-releasing peptide (GRP) at concentrations of 10(-10) and 10(-9) M in the arterial line increased the CCK output by about 100 and 500%, respectively, as measured with the assay specific for the sulphated region of CCK. Pilocarpine and physostigmine at concentrations of 10(-5) M reduced the CCK output to 24 and 40% of basal, respectively, and also abolished the GRP-stimulated CCK response. Atropine (10(-6) M) increased CCK output about 100%. The results suggest that both stimulatory and inhibitory nervous impulses may be transmitted to the intestinal CCK cell, mediated by intramural GRP neurons and cholinergic pathways, respectively.

Animals↗
PubMed1987

Bicarbonate secretion by the rabbit duodenum in vivo: effects of prostaglandins, vagal stimulation and some drugs.

Duodenal HCO-3 secretion in anaesthetized rabbits was measured by continuous titration of the recirculating luminal perfusate at pH 7.4. The segment under study started 3-4 cm distal to the pylorus and was devoid of pancreatic and biliary HCO-3 secretion. On histological examination the submucosa was seen to contain Brunner's glands, mainly of a mucous type. Duodenum in rabbit secreted HCO3- at a considerably higher basal rate (100-125 mu equiv h-1 cm-1 of intestine) than has previously been found in the rat, cat or dog. The cyclo-oxygenase inhibitor indomethacin (20 mg kg-1) reduced the secretion by 30%, while prostaglandin E2 (5-80 microM, luminal) caused a dose-dependent increase. Prostaglandins thus seem to be important in regulation of duodenal HCO3- secretion in the rabbit and may play a role in duodenal protection against acid. Carbachol (1 and 10 micrograms kg-1) and atropine (0.5 and 1 mg kg-1) had no effects whereas hexamethonium (10 mg kg-1) caused a persistent decrease (25%) in secretion. Effects of electrical stimulation of the vagal nerves or injection of the alpha 2-adrenergic agonist clonidine markedly depended on the agent used for anaesthesia. In urethane-anaesthetized animals, clonidine (0.75-75 micrograms kg-1) tended to increase the secretion whereas with nembutal, clonidine (5-150 micrograms kg-1) decreased it significantly. Electrical stimulation of the cervical vagal nerves decreased the HCO3- secretion in urethane-anaesthetized animals but had no significant effect during nembutal anaesthesia. The responses in the nembutal-anaesthetized rabbit are similar to those previously observed in the cat, rat or dog.

Adrenergic alpha-Agonists↗
PubMed1988

Acid in proximal and distal duodenum inhibits, but hyperosmolal solution does not inhibit pentagastrin-stimulated acid secretion in chronic gastric fistula rats.

In chronic gastric fistula (GF) rats, hyperosmolal 0.20 M HCl infused into a duodenal loop anastomosed to the jejunum (Roux-en-Y) produced a greater inhibition of the maximal acid response to pentagastrin than HCl or 1200 mosmol kg-1 solution of polyethylene glycol (PEG) alone, suggesting that HCl and hyperosmolal solution inhibit secretion by different mechanisms. In the present study on chronic GF rats with Thirty-Vella loops of the proximal or distal duodenum (bile and pancreatic ducts transplanted to the jejunum), perfusion of the proximal or distal loop with 0.20 M HCl significantly inhibited the maximal acid response to pentagastrin, but perfusion with hyperosmolal PEG solution did not alter the response. The results suggest different anatomical sites for the inhibitory mechanisms, sensitive to acid and hyperosmolal solution.

Animals↗
PubMed1998

Effect of VIP and PACAP on vascular and luminal release of serotonin from isolated perfused rat duodenum.

Effects of CCK, VIP, PACAP38, and PACAP27 on the release of 5HT into the intestinal lumen and into the portal circulation were examined in in vivo experiments of isolated rat duodenum perfused vascularly and luminally. VIP, PACAP 38 and 27 reduced the release of 5HT into the lumen but did not affect the vascular release of 5HT. These effects were not affected by the presence of atropine, hexamethonium, or TTX, suggesting that VIP, PACAP 38 and 27 exert a direct inhibitory effect on the luminal release of 5HT from the EC cells. Nitric oxide synthase inhibitor, NG-nitro-L-arginine, antagonized the inhibitory effects of VIP, PACAP 38 and 27, suggesting that nitric oxide seems to be essential to exert the inhibitory action of VIP and PACAPs on the release of 5HT into the intestinal lumen from the EC cells.

Animals↗
PubMed1981

Histamine receptors in the guinea-pig duodenum.

Guinea-pig duodenum contracted by histamine or by acetylcholine was relaxed dose-dependently by a series of H2-receptor selective agonists namely dimaprit, impromidine, clonidine and tolazoline. This relaxation was not neurally mediated since it was not modified by tetrodotoxin nor was it exerted through sympathetic receptors because it was not modified by pretreatment with propranolol or phentolamine. Apparently it was connected with the H2-receptor stimulation more than to peculiarities of the single compounds. However a series of H2-blocker (metiamide, cimetidine, ranitidine or oxmetidine) were unable to counteract the effect of the H2-agonists or the relaxant effect of histamine in the presence of chlorpheniramine. This peculiar situation seems to indicate the existence of anomalous H2-receptors, susceptible to the action of the agonists by not to that of the antagonists.

Acetylcholine↗
PubMedDate not supplied

Effects of cutaneous aspirin on the human stomach and duodenum.

Oral aspirin blocks cyclooxygenase in platelets, lowering serum thromboxane concentrations. Oral aspirin also blocks cyclooxygenase in the gastrointestinal mucosa, lowering prostaglandin production and increasing the risk of gastrointestinal ulceration and bleeding. Aspirin placed on the skin also inhibits cyclooxygenase in platelets, but aspirin absorption through skin is slow, which may minimize the gastrointestinal effects. Our objectives in this study were 1) to compare the pharmacokinetic and pharmacodynamic effects of cutaneous and oral aspirin in healthy volunteers and 2) to compare the effects of cutaneous aspirin on gastroduodenal mucosal prostaglandin E2 and F2 alpha content and on mucosal damage, using endoscopy. The bioavailability of cutaneous aspirin was 4%-8% that of oral aspirin. Cutaneous aspirin (750 mg/day for 10 days) significantly lowered serum thromboxane (by 85%) and gastric and duodenal prostaglandins (by 49%-71%); placebo had no effect. Moreover, cutaneous aspirin, but not placebo, resulted in significant gastric mucosal injury. These findings demonstrate that even tiny amounts of aspirin in the blood (2 microM) have inhibitory effects on prostaglandin production in the human stomach and duodenum that result in gastric mucosal damage, even without direct exposure of the stomach to aspirin.

Administration, Cutaneous↗