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Degradation of adenosine by extracellular adenosine deaminase in the rat duodenum.

1. Extracellular degradation of adenosine by adenosine deaminase was studied in the rat duodenum using high performance liquid chromatography (HPLC) and pharmacological techniques. 2. Relaxant responses to adenosine (1-10 microM) were potentiated in a concentration-dependent manner by erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) and deoxycoformycin, both of which are inhibitors of adenosine deaminase. 3. Breakdown of adenosine, determined by HPLC, due to incubation with segments of rat duodenum was inhibited by both EHNA and deoxycoformycin. Cytosolic sources of adenosine deaminase were excluded. 4. Relaxant responses to adenosine were also potentiated by the adenosine transport inhibitor dilazep, which did not inhibit adenosine deaminase activity. 5. The extracellular adenosine deaminase activity (4 units/g tissue) was high compared with activity previously determined in other organs.

Adenosine↗

Nitric oxide modulates cholinergic neurotransmission in cat duodenum.

1. Longitudinal muscle strips isolated from cat proximal duodenum were characterized by spontaneous phasic contractions. 2. Electrical field stimulation (EFS) (0.5 ms, 1-20 Hz, supramaximal voltage intensity for 40 sec) produced frequency-dependent contractions, and maximal amplitude was achieved at 10 Hz. The EFS-induced contractions were abolished either by atropine (10(-6) M) or by tetrodotoxin (3 x 10(-7) M). 3. The nitric oxide (NO) synthase blocker N infinity-nitro-L-arginine (L-NNA, 10(-4) M) or the inhibitor of the soluble guanylyl cyclase methylene blue (MB, 3 x 10(-5) M) increased the amplitude of the electrically evoked contractions. 4. L-Arginine (10(-3) M) or sodium nitroprusside (SNP, 10(-4) M) significantly decreased the amplitude of the EFS-induced, L-NNA- or MB-potentiated contractions as the effect of SNP was much more pronounced. 5. Neither L-NNA nor MB affected the contraction evoked by exogenous acetylcholine. 6. The L-NNA or MB-induced interruption of the L-arginine-NO pathway potentiated the electrically evoked cholinergic contractions, suggesting the inhibitory role of NO in the cholinergic neurotransmission realized probably at the pre-synaptic level in cat duodenum.

Animals↗

Intracellular recordings from cells in the myenteric plexus of the rat duodenum.

Intracellular recordings were made in vitro from neurons in the myenteric plexus of freshly dissected preparations of the duodenum of the rat. Nearly one-quarter of neurons (18 out of 77) had long after-hyperpolarizations following their action potentials. Over 60% of neurons (20 out of 32) which were tested exhaustively by focal stimulation at seven points around the recording site were seen to receive fast excitatory synaptic inputs. These were of very short duration (10-30 ms) and were reversibly blocked by the nicotinic antagonist hexamethonium. Only four out of 18 after-hyperpolarization cells (22%) had visible fast synaptic inputs. Seven out of 32 neurons tested received slow excitatory synaptic inputs lasting up to 60 s that were associated with a decrease in conductance and an increase in excitability. No evidence for muscarinic synaptic potentials was seen; only four cells out of 30 with fast excitatory postsynaptic potentials had slow excitatory synaptic potentials visible after a single-shot stimulus; in none of these were the slow excitatory postsynaptic potentials blocked by atropine (up to 1 x 10(-5) M). No inhibitory postsynaptic potentials were recorded in any of the 77 neurons recorded in this study. The effects of five neurotransmitter candidates (acetylcholine, GABA noradrenaline, 5-hydroxytryptamine and substance P) applied by pressure microejection were studied. It is concluded that most of the neurophysiological features reported in the extensively studied guinea-pig small bowel myenteric plexus are present in the rat duodenum. However, the apparent lack of muscarinic synaptic potentials and inhibitory synaptic potentials suggests that there may be some differences between the two species. Our recordings also differ slightly from recently reported studies of rat myenteric neurons grown in cell culture.

Acetylcholine↗

Pathologic effects of fractionated fast neutrons or photons on the pancreas, pylorus and duodenum of dogs.

Thirty-nine adult male Beagles received either fast neutron or photon irradiation to the right thorax to determine the relative biological effectiveness (RBE) of fast neutrons on normal pulmonary tissue. The right anterior abdomen was included in the field of radiation. Twenty-four dogs (six/group) received fast neutrons with an average energy of 15 MeV to total doses of 1000, 1500, 2250 or 3375 rad in four fractions per week for six weeks. Fifteen dogs received 3000, 4500 or 6750 rad of photons (five/group) in an identical fractionation pattern. All neutron irradiated dogs receiving 3375 and 2250 rad and one receiving 1500 rad developed clinical signs of pancreatic, hepatic and gastrointestinal disturbances. The liver enzymes of these dogs became elevated and they died or were euthanatized in extremis 47-367 days after irradiation. Only one 6750 rad photon dog developed similar signs and died 708 days post-irradiation. Five neutron and 10 photon exposed dogs died of other causes. Neutron-induced lesions in the stomach and duodenum included hemorrhages, erosions, ulcerations and fibrosis. Ulcers perforated the GI tract of five dogs. Pancreatic lesions included degranulation and necrosis of acinar cells, fibrosis ans atrophy. Islet cells were not obviously damaged. All lesions were associated with degenerative and occlusive vascular changes. The RBE of fast neutrons, assessed by clinical signs, gross and microscopic pathology, is approximately 3-4.5 for pancreas and about 4.5 for pylorus and duodenum.

Animals↗

Interleukin-1 modulatory effect on the action of chemotherapeutic drugs and localized irradiation of the lip, duodenum, and tumor.

PURPOSE: This study was conducted to examine the radioprotective and radiochemoprotective capabilities of interleukin 1 beta (IL-1) on two acute-reacting normal tissues of the C3H mouse, the mucosa of the lip and the duodenum. Also assessed was the modulating effect of IL-1 on tumor growth in the same strain of mice. METHODS AND MATERIALS: IL-1 was administered to C3H/Km mice in combination with fractionated irradiation, or with cyclophosphamide, cisplatin, or 5-fluorouracil (5FU) followed by irradiation. Normal tissue damage was evaluated in the mouse lip, using a subjective scoring system for tissue reaction, and in the duodenum, using the crypt cell survival assay. RIF-1 fibrosarcoma tumor response was assayed with the regrowth delay method. RESULTS: IL-1 protected against the acute reaction produced by fractionated irradiation in the lip mucosa, shifting the dose-response curve by 3.8 Gy. IL-1 was protective when injected intraperitoneally 24 hr before CY or c-DDP, which were given immediately before the first of five daily radiation dose fractions. The dose-response curves for cyclophosphamide and cisplatin were shifted 4.0 Gy and 1.6 Gy, respectively. IL-1 did not protect against 5FU toxicity when treatments were administered in that same sequence; however, when 5FU was given 4 or 8 hr before IL-1 and the first radiation dose fraction followed 20 or 16 hr later, there was significant protection and the curves were separated by 1.5 Gy or 3.5 Gy. IL-1 also protected duodenal crypt cells against the cytocidal effect of fractionated irradiation, with a dose difference of 1.5 Gy and an improvement of crypt survival of 11.7%. It was even more protective for these cells against the enhanced drug toxicity when cyclophosphamide or 5FU were administered immediately before the first of five daily radiation doses, with the dose differences of 4.4 and 5.3 Gy, respectively, and improvements of crypt survival of 33.8 and 29.9%, respectively. There was no modification by IL-1 of the effect of irradiation alone on the RIF-1 tumor. CONCLUSION: This study demonstrates the potential for use of IL-1 as an auxiliary in combinations with chemotherapeutic agents and radiation. It also indicates that for some drugs, such as 5FU, IL-1 effects may be sequence dependent.

Animals↗

Radiographic examination of the stomach and duodenum: comparison of single-, double- and biphasic-contrast methods.

We compared retrospectively three groups of 150 patients who had undergone radiologic examinations of the stomach and duodenum. Each group was examined with a different barium suspension and radiographic technique: single-contrast (SC), double-contrast (DC), or biphasic-contrast (BC). The radiographs of each study were evaluated for technical quality and visualization of lesions. The number of X-ray exposures, films, and the amount of fluoroscopic time for each study were tabulated. The total radiation dose and cost for each technique were calculated. The BC examinations required the greatest number of radiographic exposures and X-ray films; however, cost was highest for the DC method. Fluoroscopy was significantly longer during the DC procedures, and the total radiation dose was also highest with this technique. Gaseous distention and barium coating of the stomach were equally good for the BC and DC groups, but X-ray penetration of the barium suspension during compression filming was significantly better in the BC and SC groups. Areae gastricae were most frequently seen during the BC studies and artifacts from excess secretions, barium flocculation or gas bubbles were least commonly present using this technique. Significantly more lesions were demonstrated in the stomach with the BC technique than with the other methods; however, the number of lesions found in the duodenum was the same for each technique.

Adult↗

Alterations in transporter expression in liver, kidney, and duodenum after targeted disruption of the transcription factor HNF1alpha.

The transcription factor hepatocyte nuclear factor 1alpha (HNF1alpha) is involved in regulation of glucose metabolism and transport, and in the expression of several drug and bile acid metabolizing enzymes. Targeted disruption of the HNF1alpha gene results in decreased Cyp1a2, and Cyp2e1 expression, and increased Cyp4a1 and Cyp7a1 expression, suggesting these enzymes are HNF1alpha target genes. Since hepatic metabolism can be coordinately linked with drug and metabolite transport, this study aims to demonstrate whether HNF1alpha regulates expression of a variety of organic anion and cation transporters through utilization of an HNF1alpha-null mouse model. Expression of 32 transporters, including members of the Oat, Oatp, Oct, Mrp, Mdr, bile acid and sterolin families, was quantified in three different tissues: liver, kidney, and duodenum. The expression of 17 of 32 transporters was altered in liver, 21 of 32 in kidney, and 6 of 32 in duodenum of HNF1alpha-null mice. This includes many novel observations, including marked downregulation of Oats in kidney, as well as upregulation of many Mrp and Mdr family members in all three tissues. These data indicate that disruption of HNF1alpha causes a marked attenuation of several Oat and Oatp uptake transporters in liver and kidney, and increased expression of efflux transporters such as Mdrs and Mrps, thus suggesting that HNF1alpha is a central mediator in regulating hepatic, renal, and intestinal transporters.

ATP Binding Cassette Transporter, Subfamily B↗

A novel association of alveolar capillary dysplasia and duodenal atresia with paradoxical dilatation of the duodenum.

BACKGROUND/PURPOSE: The authors experienced 3 cases of persistent pulmonary hypertension of the neonate (PPHN) associated with duodenal atresia with paradoxical dilatation of the distal blind end of the duodenum. The aim of this study was to clarify the characteristics of this novel association. METHODS: The medical charts of the patients were reviewed retrospectively. RESULTS: Case 1 was a 2,862-g male infant with a prenatal diagnosis of duodenal atresia. The dilated intestine was identified as the distal blind end of the duodenum during duodeno- duodenostomy. PPHN developed after surgery, and the patient died despite treatment with inhaled nitric oxide (iNO) and extracorporeal membrane oxygenation (ECMO). Lung biopsy results showed alveolar capillary dysplasia (ACD) with misalignment of pulmonary vessels. Case 2 was a 2,244-g female infant with duodenal atresia. Surgery could not be performed because of refractory PPHN, which resulted in death. Autopsy results showed ACD with misalignment of pulmonary vessels and duodenal atresia associated with dilatation of the distal blind end. Case 3 was a 2,462-g female infant with a prenatal diagnosis of duodenal atresia associated with dilatation of the distal blind end. Enlarged echogenic fetal lungs were noted antenatally. PPHN developed after surgery, and she was extubated successfully under combined therapy with iNO and intravenous prostacyclin. Unfortunately, she finally died of refractory PPHN. A retrospective review of the prenatal ultrasonographic findings showed enlarged echogenic fetal lungs as in the first 2 cases. CONCLUSIONS: The characteristics of this novel association are enlarged echogenic fetal lungs, duodenal atresia associated with paradoxical dilatation of the distal blind end, and refractory PPHN resistant to iNO.

Capillaries↗

Cytomegalovirus infection of the graft duodenum and urinary bladder after simultaneous pancreas-kidney transplantation.

Cytomegalovirus (CMV) is an important cause of morbidity after solid organ transplantation. We report a case of CMV infection involving the transplanted duodenum that developed after simultaneous pancreas-kidney transplantation. The patient, a 30-year-old woman with insulin-dependent diabetes undergoing hemodialysis due to chronic renal failure, received a simultaneous cadaveric pancreas-kidney transplantation. The exocrine secretion was diverted using bladder drainage. Immunosuppression was maintained by a combination of tacrolimus, mycophenolate mofetil, and steroids together with OKT3 induction. Both the donor and the recipient were serologically positive for CMV IgG CMV prophylaxis consisted of a short course of parenteral gancyclovir. The patient was discharged on postoperative day 39 with normal pancreas and kidney function. She presented 2 months after transplantation with hematuria. Cystoscopic pancreas allograft biopsy specimens showed evidence of tissue invasive CMV infection in the graft duodenum and bladder. The CMV antigenemia test was positive. At 4 months after transplantation, the patient underwent surgery with the diagnosis of acute abdomen. The surgical findings consisted of a diffuse acute purulent peritonitis due to perforation of the duodenal graft. We sutured the perforation with nonreabsorbable material. The CMV antigenemia test was negative. Eight days later, the patient developed massive hematuria. At surgery, the graft was removed. The patient was discharged from the hospital with normal renal function. Pathological study of the removed graft showed the duodenal segment to have multiple wide ulcers with CMV inclusions in epithelial cells.

Adult↗

Functional expression and characterization of a sodium-dependent nucleoside transporter hCNT2 cloned from human duodenum.

We have cloned and functionally expressed a sodium-dependent human nucleoside transporter, hCNT2, from a CNS cancer cell line U251. Our cDNA clone of hCNT2 had the same predicted amino acid sequence as the previously cloned hCNT2 transporter. Of the several cell lines studied, the best hCNT2 transport function was obtained when transiently expressed in U251 cells. Na(+)-dependent uptake of [3H]inosine in U251 cells transiently expressing hCNT2 was 50-fold greater than that in non-transfected cells, and uptake in Na(+)-containing medium was approximately 30-fold higher than that at Na(+)-free condition. The hCNT2 displayed saturable uptake of [3H]inosine with K(m) of 12.8 microM and V(max) of 6.66 pmol/mg protein/5 min. Uptake of [3H]inosine was significantly inhibited by the purine nucleoside drugs dideoxyinosine and cladribine, but not by acyclic nucleosides including acyclovir, ganciclovir, and their prodrugs valacyclovir and valganciclovir. This indicates that the closed ribose ring is important for binding of nucleoside drugs to hCNT2. Among several pyrimidine nucleosides, hCNT2 favorably interacted with the uridine analogue floxuridine. Interestingly, we found that benzimidazole analogues, including maribavir, 5,6-dichloro-2-bromo-1-beta-D-ribofuranosylbenzimidazole (BDCRB), and 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), were strong inhibitors of inosine transport, even though they have a significantly different heterocycle structure compared to a typical purine ring. As measured by GeneChip arrays, mRNA expression of hCNT2 in human duodenum was 15-fold greater than that of hCNT1 or hENT2. Further, the rCNT2 expression in rat duodenum was 20-fold higher than rCNT1, rENT1 or rENT2. This suggests that hCNT2 (and rCNT2) may have a significant role in uptake of nucleoside drugs from the intestine and is a potential transporter target for the development of nucleoside and nucleoside-mimetic drugs.

Animals↗

Dynorphin-A (1-8) is contained within perikarya, nerve fibres and nerve terminals of rat duodenum.

By the use of well-characterized antibodies against porcine dynorphin-A(1-8), an endogenous opioid peptide, and the use of a modified immunofluorescence microscopic technique, dynorphin-A(1-8) stained perikarya, nerve fibres, and nerve terminals were visualized in the rat duodenum. Dynorphin-A(1-8) immunoreactive perikarya were revealed with certainty only in the myenteric plexus, while dynorphinergic nerve fibres could bee seen in the myenteric plexus and circular muscle layer, but not in the longitudinal muscle layer and submucous plexus. Dynorphin-A(1-8) immunofluorescent nerve endings were in close contacts with submucosal blood vessels, probably arterioles, and Brunner's gland cells. These findings suggest that the opioid peptide dynorphin-A(1-8) might be synthetized within myenteric plexus perikarya of the rat duodenum and that it might modulate the peristaltic activity, intestinal blood pressure, and production of mucopeptides synthetized within Brunner's gland cells.

Animals↗

Agonistic activity of SR59230A at atypical beta-adrenoceptors in guinea pig gastric fundus and duodenum.

We have recently suggested that atypical beta-adrenoceptors are present in guinea pig gastric fundus and duodenum. In the present study, we have shown that SR59230A (3-(2-ethylphenoxy)-1-[(1S)-1,2,3,4-tetrahydronaphth-1-ylamino]-(2S)-2-propanol oxalate), a selective beta(3)-adrenoceptor antagonist, possesses agonistic activities at atypical beta-adrenoceptors in these tissues. SR59230A caused concentration-dependent relaxations. However, (+/-)-propranolol (1 microM) did not affect SR59230A-induced relaxations. Pretreatment of with a combination of (+/-)-propranolol (1 microM) and the non-selective beta(1)-, beta(2)-, beta(3)- and beta(4)-adrenoceptor antagonist, (+/-)-bupranolol (30 microM), significantly antagonized the relaxant effects induced by SR59230A. The results clearly indicate that SR59230A acts as an atypical beta-adrenoceptor agonist on guinea pig gastric fundus and duodenum.

Adrenergic beta-Agonists↗

Characterization of atypical beta-adrenoceptors in the guinea pig duodenum.

The atypical beta-adrenoceptors mediating relaxation in the guinea pig duodenum were studied using catecholamines (isoprenaline, noradrenaline and adrenaline), a selective beta3-adrenoceptor agonist BRL37344 ((R*,R*)-(+/-)-4-[2-[(2-(3-chlorophenyl)-2-hydroxyethyl)amino]propyl]phe noxyacetic acid sodium salt) and a non-conventional partial beta3-adrenoceptor agonist CGP12177A ((-)-4-(3-t-butylamino-2-hydroxypropoxy)benzimidazol-2-one)). Catecholamines and beta3-adrenoceptor agonists induced concentration-dependent relaxation in this preparation. Propranolol (1 microM) produced only small rightward shifts in the concentration-response curves of these agonists. In the presence of propranolol (1 microM), however, a non-selective beta1-, beta2- and beta3-adrenoceptor antagonist bupranolol caused a concentration-dependent rightward shift of the concentration-response curves for catecholamines and beta3-adrenoceptor agonists. Schild plot analyses of the effects of bupranolol against these agonists gave pA2 values of 6.02 (isoprenaline), 5.98 (noradrenaline), 5.93 (adrenaline), 6.51 (BRL37344) and 5.70 (CGP12177A), respectively, and all Schild slopes were not significantly different from unity. These results suggest that atypical beta-adrenoceptors are present in the guinea pig duodenum and involved in mediating the functional relaxant response.

Adrenergic beta-Agonists↗

Endogenous E-type prostaglandins in regulation of basal alkaline secretion by amphibian duodenum in vitro.

Segments of proximal duodenum from Rana catesbeiana, stripped of external muscle and mounted as a tube in a glass chamber, alkalinized the luminal-side bathing solution at a rate of 1.70 +/- 0.16 microEq/cm . h (n = 18, gross surface area approximately 1.5 cm2/cm). A single change of the serosal-side bathing solution for fresh solution reduced the rate of titratable alkaline secretion, which achieved a new steady state after 45 min amounting to 66% +/- 2% of the initial rate; transmucosal potential difference (lumen negative) fell from 10.6 +/- 1.2 to 8.8 +/- 1.1 mV. Concentrations of E-type prostaglandins in the serosal-side solution measured by radioimmunoassay were 8.5 nM (3 ng/ml) before, 0.17 nM 5 min after, and 1.7 nM 90 min after the solution change (n = 8). Reapplication of the original bathing solution 90 min after the initial change reestablished original secretory rate and potential difference. The increases in alkaline secretion and potential difference were comparable in magnitude and profile to those induced by serosal administration of 10 nM prostaglandin E2. Addition of the metabolic inhibitor 2,4-dinitrophenol (100 microM, serosal side) reduced basal alkaline secretion to 30% +/- 7% of the initial rate and abolished the potential difference (n = 8). These data demonstrate that endogenous prostaglandin E production by an isolated preparation of amphibian duodenum accounts for a proportion of alkaline secretion that is equivalent to 50% of metabolism-dependent basal secretion.

2,4-Dinitrophenol↗

Intramural post-traumatic haematomas of the duodenum: are there any late sequelae of operative intervention?

The data of nine children with post-traumatic intramural haematoma of the duodenum treated in Aghia Sophia Children's Hospital of Athens from 1967 to 1980 were retrospectively analysed. Diagnosis was preoperative in all but two children, in whom diagnosis was made during laparotomy. All but one were managed by operative intervention which consisted of simple evacuation of the haematoma and closure of the serosal incision in two out of eight children. Six out of eight children operated on were followed up for 15 years, during which they were free of symptoms. Hypotonic duodenography performed in the above patients was negative for deformity or stricture of the duodenum.

Abdominal Injuries↗

Pharmacological profile of nitrergic nerve-, nitric oxide-, nitrosoglutathione- and hydroxylamine-induced relaxations of the rat duodenum.

Activation of inhibitory nonadrenergic noncholinergic (NANC) nerves in the rat duodenum cause relaxations, which are reduced by nitric oxide synthase (NOS) inhibitors indicating that this response involves a nitrergic neurotransmission. The precise nature of the nitrergic neurotransmitter is still controversial since nitric oxide (NO) scavengers and superoxide generators, even in the presence of superoxide dismutase inhibitors, failed to inhibit nitrergic neurotransmission mediated relaxations. In order to understand the role of NOS in nitrergic neurotransmission and considering that N-OH-arginine (OH-L-Arg), L-citrulline, NO, S-nitrosoglutathione (GSNO) and hydroxylamine (NH2OH) can be formed in cells during the N(G)-oxidation of L-arginine catalyzed by NOS we explored whether any of these products could exhibit biological properties comparable to those of the nitrergic neurotransmitter. After establishing which of them was able to relax the rat duodenum, the pharmacological profile of such effect was determined employing oxyhemoglobin (OxyHb), pyrogallol (PYR), hydroquinone (HQ), hydroxocobalamin (HC) or carboxy-PTIO (C-PTIO) and compared with that of nerve mediated relaxations. NO, GSNO and NH2OH, but not OH-L-ARG and L-citrulline, caused concentration-dependent relaxations that were not affected by tetrodotoxin or L-NOARG. OxyHb almost abolished NO-induced relaxations but decreased only marginally the magnitude of nerve-, NH2OH- and SNG-induced relaxations. PYR, HQ and C-PTIO reduced significantly GSNO- and NO- induced relaxations but did not affect those induced by NH2OH or nerve activation. In contrast, HC abolished NO-induced relaxations while it did not affect those induced by GSNO, NH2OH and nerve activation. The catalase inhibitor 1,2,4 aminotriazole failed to affect nerve and NH2OH induced relaxations. These findings indicate that among the products that can be formed during NOS catalyzed L-arginine N(G)-oxidation, only NH2OH caused relaxations that exhibited a pharmacological profile similar to those induced by the nitrergic neurotransmitter. Furthermore, if NH2OH is the actual neurotransmitter it appears to be acting either directly or by a catalase independent release of NO.

Animals↗

Substance P (NK1) receptor in relation to substance P innervation in rat duodenum after irradiation.

It has previously been shown that high dose of irradiation to the rat abdomen leads to an increased level of substance P (SP) in the duodenum. In the present study the pattern of distribution of NK1 receptors (NK1-R) in rat duodenum after irradiation (5-30 Gy), was examined at the same time-point (7 days) after irradiation, comparisons being made with the distribution of SP-innervation. Immunohistochemical methods were used. In controls, NK1-R-like immunoreactivity (-LI) was detected in epithelial cells, in cells in the region of the intestinal cells of Cajal within the deep muscular plexus (ICC-DMP), in neuronal cells in the myenteric plexus, and variably in granulocytes in the mucosa. Irradiation with 5-10 Gy did not lead to obvious changes in the pattern of NK1-R-LI. After irradiation with the highest doses (25-30 Gy), the mucosa was often gravely damaged, displaying granulation tissue. No epithelial NK1-R-LI was detected in this tissue, but was present in less affected mucosa after these doses. In the region of the ICC-DMP, in the myenteric plexus, and in granulocytes, NK1-R-LI was detected also after high dose irradiation. However, the degree of NK1-R-LI in the region of the ICC-DMP was somewhat lower than seen in controls and after low doses. SP-immunoreactive nerve fibers were present in the regions where NK1-R-LI was detected. These findings support a suggestion that an increased level of SP after irradiation may contribute to the dose-dependent gastrointestinal adverse effects that occur after radiotherapy.

Animals↗

[Imaging of the stomach and the duodenum].

Imaging of the stomach and duodenum provides an abundant semiology, which allows precise diagnosis. In this chapter we will review specific considerations related to CT, MRI and US imaging of the stomach and duodenum. Normal imaging features as well as the main gastric and duodenal diseases will be described and illustrated.

Duodenal Diseases↗