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Contractile and non-contractile proteins and nucleic acids in the stomach, whole jejunum and seromuscular layers of the duodenum, jejunum, ileum and large intestine in response to chronic ethanol feeding.

Rats were fed a nutritionally adequate liquid diet containing 35% of the total calories as ethanol (treated), or identical amounts of the same diet in which ethanol was replaced with isocaloric glucose (controls). At 6 weeks, rats were killed and the stomach (cardiac region), duodenum, jejunum, ileum and the large intestine (combined colon and rectum) were dissected. Seromuscular layers were prepared from the duodenum, jejunum, ileum and the large intestine. After 6 weeks of chronic ethanol feeding the wet weights of the stomach and whole jejunum were reduced by 31%. The wet weights of the duodenum, jejunum and distal ileum seromuscular layers were reduced by 19-25%. The wet weight of the large intestine seromuscular layer was unaltered. The total amounts of contractile and non-contractile protein in the small intestinal seromuscular layers were reduced by 16-52%. In jejunal serosa, the RNA contents were reduced by 29%, but total RNA contents in the serosa of the ileum and duodenum were not significantly altered. Total DNA content was reduced in jejunal and ileal serosal layers by 22 and 33%, respectively, but remained unchanged in duodenal serosa. In the stomach, total contractile and non-contractile protein was reduced by 26-52% and similarly total RNA and DNA were also decreased by 47 and 34%, respectively. Chronic ethanol feeding had no apparent effect on either contractile or non-contractile total protein, total RNA or DNA contents in colonic and rectal serosa. In the combined mucosal and seromuscular layers of the jejunum, much greater effects due to ethanol feeding were observed when compared with the jejunal seromuscular layer alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗

Traumatic injuries to the duodenum: a report of 98 patients.

Data of 98 patients who had sustained traumatic injuries to the duodenum during a recent 7-year period is reviewed. The overall mortality was 23.5%; that of the blunt injury group was 35%, that of the penetrating injury group was 20%. However, after the establishment of a trauma unit, the mortality for duodenal injuries fell from 32% to 12%. Death from duodenal wounds may be reduced by earlier hospitalization, earlier diagnosis and consequently earlier surgical repair. Vigorous treatment of shock is essential. A specialized trauma unit with personnel experienced in the management of shock and trauma problems provides a better environment to carry out the preoperative and postoperative care of the acutely injured patient. Adequate surgical treatment of the blunt injury and missile injury of the duodenum should consist of the following procedures: 1) repair of the duodenal wall utilizing conventional techniques; 2) internal decompression of the repair by afferent jejunostomy; 3) efferent jejunostomy for postoperative feeding; 4) temporary gastrostomy; and 5) external drainage of the repair. In certain selected instances, the simple stab wound of the duodenum may be treated by conventional repair without decompression, but a loop of jujunum should be sutured over the repair to prevent delayed disruption. The majority of patients with injuries to the duodenum have associated organs injured which also require considered surgical judgment and action.

Adolescent↗

Early carcinoma of the distal second part of the duodenum treated by wedge resection.

A case of early carcinoma of the distal second part of the duodenum, in a 74-year-old man, is presented. Endoscopic retrograde cholangiopancreatography was performed for diagnosis of a common bile duct stone. During this procedure, small elevated lesions were found incidentally in the distal second part of the duodenum, and the histologic examination of a biopsy specimen showed adenocarcinoma. The lesions were removed by wedge resection, and pathologic examination revealed duodenal carcinoma limited to the lamina propria. Although carcinoma of the duodenum, other than of the ampulla of Vater region, is very rare, it is sometimes possible to detect asymptomatic early tumors. However, this requires careful observation of the entire duodenal mucosa, including that of the distal duodenum, at duodenoscopy.

Adenocarcinoma↗

Patchy villous atrophy of the duodenum in childhood celiac disease.

OBJECTIVES: Patchy villous atrophy of the duodenal mucosa has been described in adults with untreated celiac disease (CD) but not in children. The authors evaluated the presence and the distribution of villous atrophy in children with celiac disease to see whether this histologic pattern exists in children. METHODS: We studied 95 children at diagnosis (Group 1) and seven during gluten challenge (Group 2). We measured anti-endomysium antibodies (EMA) by immunofluorescence on monkey esophagus, antihuman-tissue transglutaminase autoantibodies (anti-tTG Abs) by radioimmunoprecipitation, and HLA-DQ2/DQ8 heterodimers by polymerase chain reaction using specific primers. During upper intestinal endoscopy, at least five duodenal biopsy samples were obtained, one from the duodenal bulb and four from the distal duodenum. RESULTS: Thirteen of 95 (13.7%) patients in Group 1 and in 3 of 7 (42.9%) in Group 2 had patchy villous atrophy of the duodenum. In all 16 patients, villous atrophy of the bulb was present. In four children from Group 1, villous atrophy was observed only in the bulb samples. EMA, anti-tTG Abs, and HLA-DQ2/DQ8 heterodimers were present in all patients. Fourteen of 16 had symptomatic CD, and two were silent, detected during screening in subjects at risk for CD. CONCLUSIONS: This is the first study demonstrating that children with CD may have patchy villous atrophy of the duodenum. The bulb mucosa may be the only duodenal area involved, both at diagnosis and after gluten challenge. Therefore, multiple endoscopic biopsies should always be performed, not only in the distal duodenum, but also in the bulb.

Adolescent↗

Investigation of drug absorption from the gastrointestinal tract of man. I. Metoprolol in the stomach, duodenum and jejunum.

Gastrointestinal (GI) absorption of the beta-adrenoceptor blocker metoprolol was investigated in five healthy subjects by means of an intubation method, employing a triple-lumen tube introduced into the intestine, and a twin-lumen tube in the stomach. Metoprolol was introduced into the stomach with a homogenized meal containing a nonabsorbable marker, [14C]-PEG 4000, and another marker, PEG 4000, was perfused continuously into the duodenum just below the pylorus. Samples of GI contents were collected at regular intervals over 4 h in the stomach and at two different levels in the upper small intestine. Metoprolol was not absorbed from the stomach. Approximately 60% of the amount of drug emptied from the stomach was absorbed from the duodenum; about 50% of that leaving the duodenum was absorbed from the first part of the jejunum. The delivery process was the rate-limiting factor of metoprolol absorption in these segments of the gut. Plasma concentrations reflected drug loss from the lumen and were higher in subjects exhibiting faster gastric emptying and higher absorption rates in the duodenum and jejunum. The intubation technique appeared to be a suitable method for investigating drug absorption from the GI tract in man.

Adult↗

The effect of corticosteroid pretreatment in vivo on the contraction of guinea-pig ileum and duodenum.

The effects of corticosteroid pretreatment on the contraction caused by acetylcholine or electrical stimulation of guinea-pig ileum and duodenum were studied. The acetylcholine dose-response curves for steroid pretreated ileum but not duodenum were significantly shifted to the right; evidence that pretreated ileum required higher dose of acetylcholine than normal to cause 50% maximal contraction. Naloxone enhanced the contraction of normal ileum caused by acetylcholine given at the dose of ED50, but not that of normal duodenum. The dose of morphine required to abolish electrically induced contraction was higher in steroid pretreated ileum than in normal ileum. Hence, corticosteroid pretreatment may affect intestinal contractility via opioidergic mechanisms which are found in the ileum but not in the duodenum.

Acetylcholine↗

Evidence that GABAA receptors mediate relaxation of rat duodenum by activating intramural nonadrenergic-noncholinergic neurones.

GABA produced rapid and transient relaxation of rat duodenum. Homotaurine (3-aminopropansulphonic acid) but not (+/-)-baclofen had a GABA-like effect. GABA-induced relaxation was almost completely inhibited by tetrodotoxin but was unaffected by atropine. Cross desensitization developed between GABA and homotaurine but not between GABA and (+/-)-baclofen. The concentration response curve to the relaxant effects of GABA was shifted to the right by both bicuculline and picrotoxin. However maximal relaxation was still produced by GABA in the presence of bicuculline but not in the presence of picrotoxin. GABA-induced relaxation was not affected by prazosin, yohimbine, propranolol or reserpine pretreatment. Field stimulation (0.1 Hz) of rat isolated duodenum in the presence of atropine and guanethidine produced relaxation similar to that produced by GABA. The ganglionic stimulant DMPP produced a similar effect. Neither Met-enkephalin, noradrenaline, 5-HT, histamine, VIP or arachidonic acid could be held responsible for GABA-induced neurogenic relaxation of rat duodenum. ATP produced relaxations which closely mimicked those produced by either GABA or field stimulation. Exposure to ATP desensitized responses to both GABA and field stimulation to about the same extent. ATP, GABA and field stimulation-induced relaxation was unaffected by either theophylline or indomethacin, but was significantly and selectively antagonized by apamin. In conclusion, GABA-induced relaxation of rat isolated duodenum is largely dependent upon activation of intra-mural nonadrenergic-noncholinergic neurones. The GABA receptor involved appears to be of the GABAA subtype. Circumstantial evidence is provided indicating that ATP might be the endogenous substance released by GABA.

Animals↗

The electrogenic Na-pump and spontaneous contraction of the hypokalemic rat duodenum.

The effects of the electrogenic Na-pump on spontaneous contraction in the isolated, longitudinal muscle of the duodenum of rats which had been on a potassium-deficient diet for 7 weeks, have been investigated. Intracellular levels of Na+ are increased by this diet. The spontaneous contraction of the duodenal muscle was stopped, transiently, by 0.5 to 120 mM-K+ Krebs solution. The period of decrease of tone and amplitude occurring immediately after adding K+ was shortened when the external K+ concentration ([K]o) was increased from 0.5 to 120 mM. The decrease in tone and amplitude induced by K+ was abolished by exposure of the tissue to 0 mM [K]o, by exposure to a temperature below 14 degrees C, and in the presence of ouabain (3 X 10(-5)-10(-4) M). The spontaneous contraction of 'Na-rich' duodenum in bathing medium containing 15 mM K+ and following inhibition of the electrogenic Na-pump with cooling or ouabain was much the same as in the duodenum from rats fed balanced diets: i.e., increase of contractile tone immediately after adding K+. To activate the Na-pump in 'Na-rich' duodenum, the external K+ could be replaced by Rb+, Cs+, NH4+ and Tl3+. The effectiveness was in the order K+ greater than Rb+ greater than Cs+ greater than NH4+ greater than Tl3+. The possible existence of a neuronal or hormonal inhibitory mechanism affecting the active Na-K transport in rat smooth muscle in situ, under conditions of hypokalemia, is discussed.

Animals↗

Selectivity of bradykinin analogues for receptors mediating contraction and relaxation of the rat duodenum.

1. Bradykinin produces a biphasic response in the rat duodenum that consists of a relaxation (pD2 = 8.44) followed by a contraction (pD2 = 6.91). 2. The B1 agonist des-Arg9-bradykinin produced a contraction (pD2 = 7.16) but no relaxation. Des-Arg9-[Leu8]-bradykinin, which is a B1 antagonist in other systems produced contraction (pD2 = 7.65) in the rat duodenum. 3. Four bradykinin analogues that are preferential B2 agonists in other tissues had a biphasic effect with pD2 values in the range 7.22-8.68 for relaxation and 6.26-6.91 for contraction. 4. [Thi5,8,D-Phe7]-bradykinin, which is a B2 antagonist in most other systems produced relaxation in the rat duodenum, with a pD2 of 7.49. 5. It is concluded that the contractile component of the response to bradykinin in rat duodenum may be mediated by a subtype of the B1 receptor and the relaxant component by a receptor of the B2 subtype.

Animals↗

Characterization of P1-purinoceptors on rat duodenum and urinary bladder.

1. The P1-purinoceptors mediating relaxation of the rat duodenum and inhibition of contraction of the rat urinary bladder were characterized by use of adenosine and its analogues 5'-N-ethylcarboxamidoadenosine (NECA), N6-cyclopentyladenosine (CPA) and 2-p-((carboxyethyl)phenethylamino)-5'- carboxamidoadenosine (CGS 21680), as well as the A1-selective antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). The stable analogue of adenosine 5'-triphosphate (ATP), adenylyl 5'-(beta,gamma-methylene)diphosphonate (AMPPCP), was also used as previous work had indicated that it has a direct action on some P1 receptors in addition to its P2-purinoceptor activity. 2. In the rat duodenum, the order of potency of the adenosine agonists was NECA greater than or equal to CPA greater than AMPPCP = adenosine greater than CGS 21680, and DPCPX antagonized CPA and AMPPCP at a concentration of 1 nM whereas equivalent antagonism of NECA and adenosine required a concentration of 1 microM. This suggests the presence of a mixture of A1 and A2 receptors in this tissue, with CPA and AMPPCP acting on the A1 and NECA and adenosine acting on the A2 receptors. 3. In the rat bladder, the order of potency of the adenosine agonists for inhibition of carbachol-induced contractions was NECA much greater than adenosine greater than CPA = CGS 21680, and a concentration of DPCPX of 1 microM was required to antagonize responses to NECA and adenosine. This suggests the presence of A2 receptors in this tissue. ATP and AMPPCP each caused contractions which were not enhanced by DPCPX (1 microM) which suggests that in this tissue AMPPCP was acting only via P2 receptors and had no P1 agonist activity. That AMPPCP was active on the A1 receptors in the duodenum but inactive on the A2 receptors in the bladder implies that it has selectivity for the A1 subtype.4. That CGS 21680, which has been reported to bind selectively to the high affinity A2a subclass of A2 receptors, had a very low potency on the A2 receptors in the duodenum and in the bladder suggests that these receptors are of the low affinity A2b subclass.

Adenosine↗

Effect of treatment with vitamin D3 on the responses of the duodenum of spontaneously hypertensive rats to bradykinin and to potassium.

1. The diet of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) and Wistar (NWR) rats was supplemented with either 2% calcium lactate in the drinking water or 12.5 micrograms vitamin D3 100 g-1 body weight daily by gavage, for 14 days. 2. The blood pressure of the SHR treated with either calcium or vitamin D decreased to the same levels as that of WKY and NWR. 3. The response to bradykinin of the SHR isolated duodenum, which is predominantly contractile, upon treatment with vitamin D (but not with calcium), became predominantly relaxant, approaching the normal behavior of the WKY and NWR duodenum. 4. The relaxant responses of the SHR and WKY duodenum to potassium were smaller than those of NWR, but treatment with vitamin D increased the response in all three rat strains. 5. It is concluded that, besides sharing the hypotensive effect of calcium, vitamin D treatment of SHR has an effect on the duodenum smooth muscle which might be due to calmodulin-dependent activation of calcium-dependent potassium channels.

Animals↗

BK1 and BK2 bradykinin receptors in the rat duodenum smooth muscle.

1. The dual action of bradykinin (relaxation and contraction) on the rat duodenum was investigated by studying its effect on adenosine 3':5'-cyclic monophosphate (cyclic AMP) levels in cultured duodenal smooth muscle cells, and the effects of apamin on the isolated muscle responses to agonists and antagonists of BK1 and BK2 receptors. 2. No change was observed in the cyclic AMP content of cultured cells incubated with up to 100 nM bradykinin. 3. Apamin (100-500 nM) inhibited the relaxant component and enhanced the contractile component of the responses to bradykinin and to the BK2-specific analogue [Thi5,8,D-Phe7]-bradykinin. 4. Apamin (100-500 nM) did not affect the contractile response of stretched duodenum preparation to the BK1-specific agonist des-Arg9-bradykinin. 5. The BK2 antagonist, [D-Arg0Hyp3Thi5,8,D-Phe7]-bradykinin, at a concentration which completely inhibited the relaxant response to bradykinin and to [Thi5,8,D-Phe7]-bradykinin, also prevented the contraction in response to either agonist in the presence of apamin. 6. Our results demonstrate two populations of bradykinin receptors in rat duodenum: a BK2 subtype responsible for the biphasic response of the non-stretched duodenum, and a BK1 subtype responsible for the contractile effect on the stretched tissue.

Animals↗

Contractile effects of uridine 5'-triphosphate in the rat duodenum.

1. Previous studies have shown that the rat duodenum relaxes to adenosine and adenosine 5'-triphosphate (ATP) via P1 and P2Y purinoceptors respectively, but in preliminary studies uridine 5'-triphosphate (UTP) was found to contract this tissue. The non-selective P2 antagonist suramin and a number of nucleotides were therefore used to investigate this response further. 2. ATP, UTP, adenosine 5'-diphosphate (ADP), adenosine 5'-O-(3-thiotriphosphate) (ATP-gamma-S), guanosine 5'-triphosphate (GTP) and uridine 5'-diphosphate (UDP) each relaxed the duodenum, with an agonist potency order of ATP = ADP > ATP-gamma-S >> GTP >> UTP = UDP, consistent with the presence of a P2Y purinoceptor mediating relaxation. 3. ATP-gamma-S, UTP and UDP each contracted the duodenum with an agonist potency order of ATP-gamma-S > UTP > UDP, although maximal responses to these agonists were not obtained at a concentration of 267 microM (ATP-gamma-S) and 300 microM (UTP and UDP). No contractions were observed with any of the other agonists at concentrations up to 300 microM. 4. Indomethacin (25 microM) did not inhibit the contractions induced by UTP, indicating that they were not mediated via production of prostaglandins. 5. Suramin (100 microM and 1 mM) inhibited relaxations induced by ATP, shifting the concentration-response curve to the right, with the maximal response to ATP being decreased by the higher concentration of suramin (1 mM). Suramin (1 mM) inhibited relaxations induced by ATP-gamma-S, shifting the concentration-response curve to the right, and completely abolished contractions induced by ATP-gamma-S. In contrast, suramin (100 JAM and 1 mM) had no effect on contractions induced by UTP.Contractions induced by UTP were, however, less sustained in the presence of suramin, which also affected the basal tone of some tissues when precontracted with carbachol (0.1 microM). In the presence of suramin (I mM), no contractions to ATP were observed.6. These results confirm that in the rat duodenum there is a P2Y purinoceptor that mediates relaxation in response to a number of purine nucleotides, and at which the pyrimidine nucleotides UTP and UDP are almost inactive. There are also receptors at which UTP and ATP-y-S act to cause contraction.Suramin discriminates between the contractile effects of these two agonists, which may indicate the presence of a suramin-insensitive pyrimidinoceptor as well as a suramin-sensitive receptor for ATP-y-S.An alternative explanation is that the differential effects of suramin are via its actions as an antagonist in addition to its action as an ectonucleotidase inhibitor.

Adenine Nucleotides↗

Isozyme and morphological characteristics of the anaerobic fungus Piromyces mae isolated from the duodenum, rumen and faeces of sheep.

Isolates of anaerobic fungi obtained from the rumen, duodenum and faeces of sheep were identified as Piromyces mae based on their morphological characteristics observed using light microscopy. There was no significant morphological variation among the isolates of P. mae from the rumen, duodenum and faeces. Isozymes of 12 isolates of P. mae (one each from the rumen, duodenum and faeces from 4 different sheep) were analysed by PAGE. A total of 12 isozymes were studied and 5 isozyme loci were successfully typed. They were malic enzyme, malate dehydrogenase, shikimate dehydrogenase, alpha-esterase and beta-esterase. All the isolates of P. mae regardless of whether they were from the rumen, duodenum or faeces or from different animals produced very similar isozyme banding patterns for each of the enzyme systems. The similar isozyme profiles of the isolates indicate that they are of the same species although they exist in different regions of the alimentary tract.

Anaerobiosis↗

Carbonic anhydrase in the normal rat stomach and duodenum and after treatment with omeprazole and ranitidine.

A low pH in the lumen of the stomach and duodenum stimulates gastroduodenal mucosal secretion of bicarbonate, particularly in the duodenum. Long-term deprivation of this acid stimulus might affect the ability of the mucosa to secrete bicarbonate, with a consequent decrease in mucosal protection against the acid. This could occur by 'down-regulation' of carbonic anhydrase (CA) activity in the bicarbonate-transporting cells. Levels of CA activity and amounts of CA isoenzymes in rat gastric and duodenal mucosa were determined by biochemical assay and histochemical and immunohistochemical staining. Control animals and animals pre-treated for 4-6 weeks with the histamine H2-receptor antagonist ranitidine (600 mg kg-1 daily) or the H+,K+-ATPase inhibitor omeprazole (28 mg kg-1 daily) were examined. Both drugs are potent inhibitors of gastric secretion of acid. Both gastric and duodenal mucosal total CA activity and the distribution of isoenzymes were very similar in control animals and animals treated with these drugs. In the stomach, CA II was found in the surface epithelial and parietal cells. In the duodenum both CA I and CA II were observed. The staining for CA I was restricted to a small number of villus cells which looked like ordinary duodenal enterocytes. CA II in the duodenum was found in all villus cells, except the goblet cells. The staining decreased gradually from the top to the bottom of the villi and was absent in the crypts. Duodenal bicarbonate secretion is dependent on mucosal CA activity, and the distribution of CA II thus suggests that this alkaline secretion is of villous rather than cryptal origin.

Animals↗

Intramural neural pathways between the duodenum and sphincter of Oddi in the Australian brush-tailed possum in vivo.

1. Balloon distension of the duodenum 2 cm oral or anal to the sphincter of Oddi-duodenal junction elevated the amplitude of spontaneous sphincter of Oddi phasic contractions by 37.7 +/- 8.5 or 120.1 +/- 79.8%, respectively (mean +/- S.E.M., both n = 6, P < 0.05, Wilcoxon test). To further investigate this response, this study aimed to determine if: (i) electrical field stimulation (EFS) of the duodenum influences sphincter of Oddi activity; (ii) intramural nerves mediate the response; and (iii) nicotinic and/or muscarinic receptors are involved. 2. Electrical field stimulation (70 V, 0.5 ms; 5-60 Hz, 10-20 s) of the duodenal anterior serosal surface 2-4 cm oral or anal to the sphincter of Oddi-duodenal junction, produced excitatory responses in the sphincter of Oddi in anaesthetized Australian brush-tailed possums (n = 45). 3. These responses were frequency dependent, maximal at 30 Hz (n = 4) and abolished by tetrodotoxin (9 micrograms kg-1 I.A.; n = 6), or by crushing the duodenum (n = 3). Hexamethonium bromide (30 mg kg-1 I.V.) did not significantly alter the response to duodenal EFS either oral (n = 6) or anal (n = 8) to the sphincter of Oddi-duodenal junction. Atropine sulphate (30 micrograms kg-1 I.V.) reduced the response to duodenal EFS oral and anal to the sphincter of Oddi-duodenal junction to 11.2 +/- 5.8 (n = 6) and 45.0 +/- 26.8% (n = 8), respectively (both P < 0.05). 4. Bilateral cervical vagotomy and guanethidine infusion (10 mg kg-1 over 15 min I.V.) did not significantly alter the responses to duodenal EFS (n = 7). 5. Excitatory intramural neural pathways between the sphincter of Oddi and the segment of duodenum 4 cm oral and anal to the sphincter of Oddi-duodenal junction have been demonstrated. These postganglionic pathways may involve muscarinic receptors.

Animals↗

Patterns of colonisation of Campylobacter pylori in the oesophagus, stomach and duodenum.

Thirty five subjects underwent upper gastrointestinal endoscopy and multiple biopsy (30 patients, five normal subjects). A total of 11 biopsies per subject from four sites (oesophagus (three), gastric body (two), antrum (three), duodenum (three] were examined for inflammation and the presence of Campylobacter pylori and using standard methods of culture and by light (LM) and electron microscopy (EM). The organism was cultured from oesophageal biopsies in eight of 30 (27%) patients but could not be identified at this site by LM or EM. There was evidence of oesophageal inflammation in 20 patients which was associated with the local finding of C pylori in five (25%) including two of seven (29%) with Barrett's mucosa. Antral C pylori was present in 22 of 23 (96%) patients with chronic active gastritis. The organism was found in the antrum and oesophagus in four of 22 patients (18%), in the antrum and duodenum in four of 22 patients (18%) and in all three sites in a further two of 22 patients (9%). Antral C pylori was found in five of six patients with peptic ulceration. C pylori was cultured from the duodenum in six patients with confirmation by LN and EM in three, but only on areas of gastric metaplasia. The organism was not found in the normal group. This study indicates that C pylori may be irregularly isolated from the oesophagus and duodenum in patients with antral C pylori and chronic active gastritis. The role of C pylori in the oesophagus is most likely that of a commensal or contaminant.

Adult↗

Sensory and biomechanical responses to ramp-controlled distension of the human duodenum.

The aim of this study was to develop a new method for investigation of the relationship among the mechanical stimulus, the biomechanical properties, and the visceral perception evoked by volume/ramp-controlled distension in the human duodenum in vivo. An impedance planimetric probe for balloon distension was placed in the third part of the duodenum in seven healthy volunteers. Distension of the duodenum was done at infusion rates of 10, 25, and 50 ml/min. The pump was reversed when level 7 was reached on a visual analog scale ranging from 0 to 10. Distensions were done with and without the administration of the antimuscarinic drug butylscopolamine. The total circumferential tension (T(total)) and the passive circumferential tension (T(passive)) were determined from the distension tests without and with the administration of butylscopolamine, respectively. T(total) and T(passive) showed an exponential behavior as a function of strain (a measure of deformation). The active circumferential tension (T(active)) was computed as T(total)-T(passive) and showed a bell-shaped behavior as a function of strain. At low distension intensities, the intensity of sensation at 10 ml/min was significantly higher than that obtained at 25 and 50 ml/min. The coefficient of variation at the pain threshold for circumferential strain (average 4.34) was closer to zero compared with those for volume (8.72), pressure (31.22), and circumferential tension (31.55). This suggests that the mechanoreceptors in the gastrointestinal wall depend primarily on circumferential strain. The stimulus-response functions provided evidence for the existence of low- and high-threshold mechanoreceptors in the human duodenum. Furthermore, the data suggest that high-threshold receptors are nonadapting.

Adult↗