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Myoelectric activity in the stomach and duodenum after epidural administration of morphine or bupivacaine.

BACKGROUND: Gastric emptying is delayed in patients receiving postoperative pain relief with epidural morphine compared to patients receiving epidural bupivacaine. The electrophysiological basis for this effect is unknown. The aim of this study was to compare the effects of epidural morphine with epidural bupivacaine on gastroduodenal myoelectric activity (EMG) in patients after surgery. METHODS: Fourteen patients with epidural analgesia who underwent open cholecystectomy were randomly assigned to receive either epidural morphine (EM) or epidural bupivacaine (EB) for postoperative pain relief. During surgery EMG electrodes were placed in the subserosa in the antrum and duodenum and the EMG registration started 3.5 hours after the end of surgery. Gastric emptying measured with the acetaminophen test was studied in the morning the day after surgery. RESULTS: The spike activity in the antrum was significantly lower 160-340 minutes after the administration of morphine in the EM-group compared to the activity in the EB-group (P < 0.04). The incidence of regular slow wave rhythm in the antrum was significantly lower 160-520 minutes after the administration of morphine in the EM-group compared to the EB-group (P < 0.03). Duodenal Phase III activity measured with EMG was significantly more frequent during 160-520 minutes after the morphine administration in the EM-group compared to the EB-group (P < 0.02). The acetaminophen absorption was significantly delayed in the epidural morphine group compared to the epidural bupivacaine group. CONCLUSIONS: Gastroduodenal electromyographic activity was significantly changed during epidural morphine compared to epidural bupivacaine. The delayed gastric emptying during epidural morphine may be explained by decreased and uncoordinated contractile activity in the antrum, shown by decreased spike activity and irregular slow wave rhythm. The increased pressure activity in the duodenum, shown by increased Phase III activity, may also impair gastric emptying.

Adult↗

Electromyography of the reticulum, abomasum and duodenum in dairy cows with left displacement of the abomasum.

Electromyographic (EMG) recordings of the reticulum, abomasal corpus, pyloric antrum and duodenum of six dairy cows with left displacement of the abomasum (LDA) were made in order to substantiate abomasal atony as a prerequisite to abomasal displacement. EMG recordings were made when LDA was present as well as when absent. Mean values were determined in five of six cows for the maximum peak or amplitude, mean peak values, peak-to-peak interval and count of the electrical response activity (ERA) for each 15 min segment of the waveform recordings. Segments containing phase III migrating myoelectric activity were not analysed. LDA positive periods were compared to LDA negative periods in each cow. The 6 h period (transition period) prior to the diagnosis of LDA was analysed separately. Paired t-tests were applied to group values with statistical significance established at the P = 0.05 level. There was a significant decrease in the ERA count during the LDA positive periods in the abomasal corpus (-1.40% to -7.88%, P = 0.0217) and in the pyloric antrum (-2.05% to -11.98%, P = 0.0430). A corresponding significant increase occurred in the peak-to-peak interval. During the transition period spike activity in the duodenum increased 0.5% to 48.31% (P = 0.0474) and the peak-to-peak interval was significantly decreased. No extended periods of atony were observed in the abomasum during this study.

Abomasum↗

Anomalous peritoneal folds of the duodenum--a normal variant simulating disease.

The double contrast barium meal appearance of four cases is presented where an anomalous peritoneal fold involves the duodenum. This fold results in a characteristic smooth, extrinsic indentation upon the antero-superior surface of the duodenal cap. This normal variant should be differentiated from distortion of this region due to pathology such as peptic ulceration. Anomalous peritoneal folds which involve the duodenum (cystoduodenal ligament, cysto-gastrocolic ligament) are not believed to cause symptoms (1). However, the recognition of the deformity produced by these folds is important, requiring differentiation from pathological changes.

Barium Sulfate↗

Modulation of electrically evoked responses in rat duodenum by activation of nicotinic cholinoceptors.

1. The effect of activation of nicotinic cholinoceptors in rat duodenal segments following electrical field stimulation (EFS) was investigated. 2. Electrical field stimulation elicited a two-component response: transient relaxation followed by contraction. The EFS-evoked response was tetrodotoxin (TTX; 1 mumol/L) sensitive. The relaxation component was NG-nitro-L-arginine (L-NNA; 100 mumol/L) sensitive, while the contractile response was atropine (1 mumol/L) sensitive. 3. 1,1-Dimethyl-4-phenyl-piperazinium iodide (DMPP; 20 mumol/L) induced relaxation of spontaneously active preparations that was L-NNA sensitive. L-Arginine (1 mmol/L) reversed the effects of L-NNA on DMPP-induced relaxation. 4. When EFS was applied, DMPP increased the amplitude of the relaxation component of the response and reduced the contractile component. 5. In the presence of L-NNA, the effect of DMPP on the relaxation component of the response to EFS was reduced, but the contractile response was not affected. L-Arginine partly reduced this effect of L-NNA. 6. Neither propranolol (1 mumol/L) nor yohimbine (1 mumol/L) had any effect on the actions of DMPP on EFS-evoked responses, but prazosin (1 mumol/L) strongly reduced the effect of DMPP on the contractile component of the response to EFS and slightly reduced the effect of DMPP on the relaxation response. 7. Histochemical studies demonstrated that, in the myenteric plexus of the rat duodenum, there are many reduced nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d)-positive neurons and that their number decreased after treatment with L-NNA. In the presence of L-arginine and L-NNA, the number of NADPH-d-positive neurons was similar to that found in control samples. 8. The data suggest that activation of nicotinic cholinoceptors modulates EFS-evoked responses in the rat duodenum as a result of the potentiation of nitrergic and adrenergic neurotransmission.

Action Potentials↗

In vivo cell kinetics studies of the duodenum during and after healing of cysteamine-induced duodenal ulcer in rats using bromodeoxyuridine incorporation.

The present study investigated the defect of duodenal defence responsible for the tendency of recurrence of duodenal ulcer. Male Wistar rats were treated with cysteamine-HCl subcutaneously to induce duodenal ulcer, and bromodeoxyuridine (BrdU) was given intraperitoneally 1 h before laparotomy. Serial tissue sections and immunocytochemical staining of BrdU were done to study the cell kinetics during and after healing. Deep ulcers developed in the proximal part of the duodenum 24 h after cysteamine injection, and the ulcer was replaced by scar tissue 1 week later. BrdU-labelling index of normal duodenal mucosa in control rats was 30-34%. On the peripheral part of the regenerative mucosa, BrdU-labelling index increased from 1.5% to 26-27%, 1-4 weeks after injection and remained at this level thereafter. On the central part, except the most central area, the labelling index remained at 0% until 3 weeks, and was 15% 6 weeks after cysteamine treatment. It never achieved the level seen in control normal mucosa. The labelling rate of fibrous cells in scar tissue decreased from 28% to nearly 0% 1-4 weeks after the injection. It is concluded that both the ulcer scar and the regenerative mucosa do not achieve a mature state in the initial scarred stage; they need more time to reach a relatively mature condition. Moreover, the regenerative mucosa will be the weak, easily damaged part of the duodenum.

Animals↗

Carcinoid tumor arising in a duplication cyst of the duodenum.

Reported herein is a case of carcinoid tumor arising in a duplication cyst of the duodenum in a 34-year-old woman. Ultrasonography at a health check-up revealed a 10 cm cystic mass located in the retroperitoneum adjacent to the third portion of the duodenum. Macroscopically, it had a smooth surface without communication with other organs and was filled with brownish necrotic fluid. More than half of the inner wall was occupied by a white, irregular, and solid nodule, which protruded into the lumen. The nodule was diagnosed as a carcinoid tumor invasive to the deep muscular layer. The non-neoplastic cyst wall had bowel structures including mucosa, submucosa and double layers of smooth muscle, indicating that the lesion was a duodenal duplication cyst. Most of the mucosa was eroded by marked inflammation. The remaining mucosa consisted of various types of epithelium, the major type having the nature of primitive gastric mucosa. Of interest was the presence of hamartomatous components in the wall. Furthermore, the non-neoplastic mucosal lining cells around the carcinoid tumor expressed neuroendocrine antigens and had minimal proliferative activity, suggesting that part of the cyst wall provided a microenvironment for accelerated differentiation of epithelial cells to an endocrine phenotype and transformation to neoplasia.

Adult↗

Involvement of P1-purinoreceptors in the relaxing effect of adenosine in rat duodenum.

1. In isolated segments of rat duodenum, adenosine (50 microM-2 mM) caused a very rapid and short-lasting relaxation that was associated with a marked decrease in the amplitude of spontaneous contractions. 2. Theophylline (0.1-0.8 mM) and 8-phenyltheophylline (1-10 microM) antagonized, in a concentration-dependent manner, the effects of 0.3 mM adenosine on smooth muscle tension and spontaneous activity. 3. The concentration-response curves for adenosine (50 microM-2 mM) were progressively shifted to the right by increasing concentrations of theophylline and of 8-phenyltheophylline, with no change in the maximum effect. 4. 8-Phenyltheophylline (5 microM) did not affect relaxations induced by noradrenaline (0.5 microM) and by isoprenaline (5 nM). 5. These results indicate that the effects exerted by adenosine on rat duodenum are mediated by P1-purinoreceptors.

Adenosine↗

Influence of GABA and ethylenediamine in the guinea-pig duodenum.

1. GABA induced concentration-dependent transient contractions of the guinea-pig duodenum, but only occasionally evoked small relaxatory responses. The GABA-induced contractions were blocked by atropine and tetrodotoxin but were not influenced by hexamethonium; during electrically evoked twitch contractions, GABA had a concentration-dependent inhibitory effect. 2. The concentration-response curve for the contractile effect of GABA was shifted to the right in a dose-dependent manner by bicuculline and picrotoxin, with a clear reduction of the maximal effect in the presence of picrotoxin. 3. Homotaurine and delta-aminovaleric acid but not baclofen mimicked the GABA-induced contractions; the responses induced by these GABAA receptor agonists were antagonized by atropine, tetrodotoxin and bicuculline. Baclofen concentration-dependently inhibited electrically evoked twitch contractions. 4. Ethylenediamine also had a GABA-like effect, and cross-desensitization developed between GABA and ethylenediamine. 5. The ethylenediamine-induced contractions were not antagonized by thiosemicarbazide; they were reduced by 3-mercaptopropionic acid but the GABA-induced contractions were reduced to the same extent. 6. It is concluded that GABA induces contraction of the guinea-pig duodenum by excitation of GABAA receptors on postganglionic cholinergic neurones; a GABAB receptor-mediated inhibitory effect can be observed during electrically evoked twitch contractions. Ethylenediamine mimicks the GABAA receptor-mediated effect probably by a direct effect on the GABAA receptors.

3-Mercaptopropionic Acid↗

On the peptidergic hypothesis for non-adrenergic non-cholinergic innervation in the rat duodenum.

1. The nature of the non-adrenergic, non-cholinergic (NANC) transmitter was studied in vitro in the rat duodenum, by use of an isometric-isovolumic preparation. 2. Electrical field stimulation (EFS) induced a tetrodotoxin (TTX)-sensitive fall both in luminal pressure and in isometric tension. 3. Neurotensin (NT) induced TTX-insensitive inhibitory responses similar to those induced by EFS. Vasoactive intestinal peptide (VIP) caused a delayed, slow, concentration-dependent, TTX-insensitive inhibitory effect, detected only by a change in luminal pressure. 4. alpha-chymotrypsin prevented the NT- and VIP-induced inhibitory effects and antagonized the response to EFS. 5. Apamin antagonized the EFS- and NT-induced effects, but failed to affect the relaxation in response to exogenous VIP. 6. Desensitization of NT receptors by exposure to NT (10 nM) for 30 min did not affect the EFS-induced relaxation. 7. These findings provide support for the involvement of a peptide in the NANC relaxation in rat duodenum. However, there is no evidence that NT or VIP are neurotransmitters released from the NANC system in this preparation.

Animals↗

Some effects of dipyridamole, hexobendine and lidoflazine on inhibitory processes in rabbit duodenum.

Some of the effects of dipyridamole, hexobendine and lidoflazine on mechanical responses in rabbit duodenum have been investigated. In concentrations known to inhibit tissue accumulation of adenosine and its metabolites, none of these agents potentiated inhibitory responses to intramural nerve stimulation or to application of adenosine, adenosine triphosphate or phenylephrine. These results neither support nor dispute the suggestion that adenosine or a related nucleotide is the intramural inhibitory transmitter but do show that tissue accumulation in rabbit duodenum is not an important feature in the termination of the action of adenosine.

Adenosine↗

The action of porcine glucagon on the motility of the canine duodenum and jejunum.

1 Intravenous bolus doses of porcine glucagon of 0.001-0.05 mg kg-1 caused intense stimulation of the duodenum and jejunum of the dog. 2 Intravenous infusion of porcine glucagon at 0.025-0.05 mg kg-1 h-1 caused similar stimulation. In both cases the stimulation was phasic in nature. 3 Stimulation of the duodenum and jejunum following glucagon was accompanied by a decrease in frequency of the intestinal basic electrical rhythm (BER). No change was seen in the intervals between successive periods of phase III motor activity.

Animals↗

Further evidence for the existence of two receptor sites for bradykinin responsible for the diphasic effect in the rat isolated duodenum.

Low doses of bradykinin (below 10 nM), as well as of K+ (below 10 mM) induced relaxation, whereas higher doses caused contraction of the rat duodenum. The relaxant responses induced by bradykinin and K+ were not affected by ouabain (1 microM), but pre-incubation with 5.9 mM K+ abolished the responses to that ion but not those to bradykinin. The contractile and relaxant components of the response to bradykinin (but not those to K+) increased with the time elapsed after mounting of the preparation, and this was due to stretching by the load of the recording system. Specific and reversible desensitization (tachyphylaxis) was observed with the contractile response (but not the relaxation) induced by bradykinin. Des-Arg9-bradykinin, an analogue specific for B1-receptors, was much less active than bradykinin, and elicited only a contractile response. Among four bradykinin potentiating peptides that were tested, potentiator C enhanced the relaxation only, whereas BPP5a and captopril potentiated only the contraction and BPP9a potentiated both types of response to bradykinin. Our results support the hypothesis that the relaxant and contractile components of the rat duodenum's response to bradykinin are due to actions at different receptor sites, which can be distinguished by their properties (desensitization) and their different apparent affinities for agonists and for potentiating peptides.

Animals↗

Evidence that tachykinin NK1 and NK2 receptors mediate non-adrenergic non-cholinergic excitation and contraction in the circular muscle of guinea-pig duodenum.

1. In the presence of atropine (1 microM), guanethidine (3 microM), indomethacin (3 microM), apamin (0.1 microM) and L-nitroarginine (L-NOARG, 30 microM), electrical field simulation (EFS) produced a nonadrenergic, noncholinergic (NANC) excitatory junctional potential (e.j.p.), action potentials and contraction of the circular muscle of the guinea-pig proximal duodenum, recorded by the single sucrose gap technique. 2. The selective tachykinin (TK) NK1 receptor antagonist, GR 82,334 (30 nM-3 microM) produced a concentration-dependent inhibition of the EFS-evoked NANC e.j.p. and contraction. Similarly, the selective NK2 receptor antagonists, MEN 10,627 (30 nM-3 microM) and GR 94,800 (100 nM-10 microM), both produced a concentration-dependent inhibition of the EFS-evoked NANC e.j.p. and contraction. GR 82,334 inhibited the electrical and mechanical NANC responses to EFS in an almost parallel manner, while MEN 10,627 and GR 94,800 were more effective in inhibiting the mechanical than the electrical response to EFS. 3. Activation of the NK1 or NK2 receptor by the selective agonists, [Sar9]substance P (SP) sulphone and [beta Ala8]neurokinin A (NKA) (4-10), respectively (0.3 microM each), produced depolarization, action potentials and contractions. GR 82,334 selectively inhibited the responses to [Sar9]SP sulphone, without affecting the responses to [beta Ala8]NKA (4-10). MEN 10,627 and GR 94,800 inhibited or abolished the responses to [beta Ala8]NKA (4-10), without affecting the responses to [Sar9]SP sulphone. 4. Nifedipine (1 microM) abolished the action potentials and contraction produced either by EFS or by the TK receptor agonists [Sar9]SP sulphone or [beta Ala8]NKA (4-10). 5. In the presence of nifedipine, the NANC e.j.p. produced by EFS was biphasic: in the majority of strips tested (21 out of 29) an early fast phase of depolarization was followed by a second slow component. The combined administration of GR 82,334 and GR 94,800 (3 microM each) reduced both components, the slow phase being inhibited to a greater extent than the fast phase. 6. The P2 purinoreceptor antagonist, suramin (100 microM) reduced the fast phase of the e.j.p. produced by EFS in the presence of nifedipine, without affecting the slow phase. The combined administration of suramin, GR 82,334 and GR 94,800 produced a nearly complete blockade of the e.j.p. produced by EFS in the presence of nifedipine. 7. When tested in the absence of apamin and L-NOARG, EFS induced a NANC inhibitory junction potential (i.j.p.) followed by an e.j.p., and the selective P2Y receptor agonist, adenosine-5'-O-(2-thiodiphosphate) (ADP beta S, 10 microM), produced membrane hyperpolarization. After addition of apamin and L-NOARG, the ij.p. was blocked, and EFS produced a pure NANC e.j.p.; ADPPS produced depolarization, action potentials and contraction.8. Suramin (100 microM) blocked the depolarization, action potentials and contractions produced by ADP beta S in the presence of apamin and L-NOARG, without affecting the responses produced by the NK1receptor agonist, [Sar9}SP sulphone.9. We conclude that NK1 and NK2 receptors cooperate in producing NANC excitation and contraction of the circular muscle in the guinea-pig proximal duodenum. Activation of either TK receptor produces membrane depolarization and both receptors contribute to generate action potentials which are essential for producing muscle contraction, via nifedipine-sensitive calcium channels. It appears that endogenous ATP chiefly acts as an inhibitory transmitter but, after blockade of NANC inhibitory mechanism(s),ATP may act as a fast signalling excitatory transmitter.

Action Potentials↗

Granular cell tumor of the duodenum: a case report.

Granular cell tumor (GCT) in the duodenum is an extremely rare disease: only one case has been listed in a review, to date. We reported a 47-yr-old Japanese male case with GCT of the duodenum. Clinically, melena caused by bleeding from the tumor was the only symptom. The tumor cells showed abundant, granular eosinophilic cytoplasm. Although this tumor was clinically and histologically benign, highly developed tumor microvessels were demonstrated both angiographically and histologically, suggesting malignant potential of the tumor.

Duodenal Neoplasms↗

Acid in the duodenum.

Acid in the duodenum triggers many physiological responses. Also, acid in the duodenum elicits hyperalgesia of the foregut. In the article by Hobson et al. in this issue the reduction of the latencies in evoked potential in response to electrical stimulation of the esophagus after duodenal acidification is reported, which may explain the symptom development in functional dyspepsia. Microscopic damages of the duodenal epithelium might be responsible for such changes. Microscopic damages of the intestinal epithelium may come into the center stage of the pathogenesis of functional GI disorders.

Duodenum↗

Villus tip microcirculation in the rat duodenum.

Duodenal microvascular perfusion was measured in anaesthetized rats both as erythrocyte velocity (rcv) in capillaries in the tip of duodenal villi and by laser-Doppler flowmetry (LDF). Rcv increased transiently by about 40% during the first 5 min of luminal exposure to 10 mM (NaCl to isotonicity) hydrochloric acid, while LDF measurements only showed a transient increase of about 7%, followed by a prolonged reduction by about 11%. Since the LDF signal is a measure not only of villus microcirculation but also of blood flow in the deeper layers, our results may suggest that blood flow is transiently redistributed towards the villi from deeper layers. Hypovolaemia (bleeding by approximately 10% of the blood volume) reduced rcv in the capillaries by 63% during the first 5 min of hypotension, but reduced LDF only by about 12%, a discrepancy which suggests a shift in blood flow from the tip to deeper layers. The experiments were performed under atmospheric oxygen tension, but rcv in the villus capillaries exposed to abdominal PO2 (approximately 45 mmHg) did not differ significantly from the values obtained under the atmospheric oxygen condition, either in the resting situation or during hypotension. In conclusion, we have developed an animal model in which red cell velocity in the tip of the duodenal villi can be studied for several hours and in which alkaline secretion from the duodenum is similar to previously reported levels. Our results show that the villus tip microcirculation in the duodenum may respond differently from that of deeper layers of the duodenal wall.

Animals↗

Evaluation of contraction time and recovery period as a parameter in the calcium antagonistic action on the K(+)-depolarized rat duodenum.

Verapamil, nifedipine, phentolamine, tolazoline, gentamicin and neomycin inhibited calcium-induced contractions of K(+)-depolarized duodenum of rat by shifting the concentration-response curves to the right. Non-competitive inhibitions were observed with trifluoperazine, lidoflazine, procaine and tetracaine. Lanthanum behaved as a partial agonist in this preparation, while nitroprusside was ineffective. Contraction times in the presence of the antagonists and recovery time of the Ca2+ responses after the removal of the antagonists from the bathing medium were evaluated. From the findings, it is suggested that the contraction time and the time required for tissue recovery after removal of a Ca2+ antagonist are parameters making K(+)-depolarized rat duodenum a potential tool for the evaluation of the pharmacological effects of Ca2+ antagonists.

Animals↗

The effect of Ca2+ antagonists on spontaneous motility from sheep duodenum.

Longitudinal smooth muscle of the sheep duodenum showed a rhythmic spontaneous activity with an average frequency of 5.6 +/- 0.55 phasic movements min-1 and a mean value of the amplitude of phasic contractions of 0.956 +/- 0.1 g. When the strips were incubated in Ca(2+)-free medium, the spontaneous motility amplitude (SMA) was reduced to 37 +/- 8.2% of control values. In Ca(2+)-free medium plus EDTA (1 or 2 mM), the SMA was strongly reduced to 21.9 +/- 8.3 and 1.8 +/- 1.8%, respectively. Verapamil, nifedipine and diltiazem diminished the SMA. The EC50 value for verapamil was 10(-9) M, whereas that for diltiazem was 2 x 10(-9) M and for nifedipine was 3 x 10(-14) M. Trifluoperazine and TMB-8 reduced the SMA with EC50 values of 7 x 10(-6) and 3 x 10(-5) M, respectively. The spontaneous activity in the sheep duodenum seemed to be mediated by influx extracellular Ca2+, which enters through potential-dependent channels and intracellular Ca2+ release.

Animals↗