[Adaptation of the intestine following extensive small intestine resection].
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Adaptation, Physiological↗
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[Scanning electron microscopic studies on the experimental ulcer of the rat small intestine. I. Micro-angiological observation on the healing process of the small intestinal ulcer by the injection replica scanning electron microscope method (author's transl)].
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Animals↗
Prolonged ambulatory small intestinal and colonic motility monitoring: potential in irritable bowel syndrome--first report of prolonged ambulatory oesophageal, small intestinal and colonic motility in the same patient.
Irritable bowel syndrome (IBS), which affects up to 25% of the population in western countries and accounts for up to 50% of referrals to gastroenterologist, remains mainly a diagnosis of exclusion. We have studied, for the first time, prolonged ambulatory motility recordings from the oesophagus, small intestine and colon of a patient who was referred to us with a 12-year history of abdominal pain and a presumptive diagnosis of IBS. The results indicated that the diagnosis was pseudo-obstruction syndrome rather than IBS. Wider clinical use of the new techniques of prolonged ambulatory intestinal motility monitoring in IBS would offer considerable potential not only in achieving a greater understanding of its pathophysiology but also in providing a more precise definition of clinical and therapeutic subgroups.
Colon↗
Intestinal function following allogeneic small intestinal transplantation in the rat.
This study tests the hypothesis that small bowel transplantation alters the function of the intestine. The function of the small intestine was investigated after syngeneic (BN----BN or Lew----Lew) and fully allogeneic (BN----Lew) orthotopic total small intestinal transplantation (SIT) using a two-stage model. All animals were treated with cyclosporine A throughout the 60-day study period. Syngeneic transplantation reduced weight gain in the (BN----BN) rats, but not in the (Lew----Lew) animals. Allogeneic transplantation caused a reduction in weight gain for the first 30 days posttransplantation, which may have been associated with graft-versus-host disease. Thereafter, the rate of growth of allogeneic SIT animals was normal. Dietary fat absorption was reduced in all groups of transplanted animals. Intestinal permeability to mannitol and polyethylene glycol 400 (PEG-400) was increased by syngeneic transplantation in all groups, with further permeability increases to mannitol, lactulose, PEG-400, and 51Cr-EDTA after allogeneic SIT. The glucose-stimulated intestinal short circuit current was reduced by both syngeneic and allogeneic SIT, but the maximal active transport rate for glucose uptake was increased, as was the passive uptake of fatty acids. These functional alterations were not associated with changes in intestinal morphology or evidence of rejection. These findings demonstrate that: (1) SIT results in significant changes in the transport characteristics of the bowel, but these have a minimal impact on the well-being of the animal overall; (2) SIT induces an increase in intestinal permeability to mannitol and PEG-400, with a further increase in permeability to all markers following allogeneic SIT; (3) following SIT, and the immune events associated with allogeneic SIT, significant adaptation of the transplanted intestine occurs. We suggest that denervation of the small intestine after SIT is the underlying cause of the changes observed.
Animals↗
In vivo zinc transport by rat small intestine after extensive small bowel resection.
We studied the effects of intestinal resection on in vivo zinc transport and intestinal tissue zinc in remnant duodenum and ileum 4 wk after two-thirds small bowel enterectomy. In situ duodenal and ileal intestinal segments from resected and sham-operated control rats were perfused through the lumen with an isotonic solution containing 0.077 mM zinc with isotopic 65Zn as tracer. After resection there was significant mucosal growth in both segments, but segment transport specific activities (transport per gram mucosa) were unchanged. Therefore, increased segment transport capacities (transport per centimeter segment length) in both segments approximated increased mucosal mass. Comparisons with transport data from our earlier studies on other luminal substrates in rats after small bowel resection showed that adaptive transport mechanisms vary not only with the luminal substrate examined but may also differ in remaining proximal and distal small bowel. In the present study about 12% of the absorbed radiotracer zinc remained in the intestinal wall after perfusion of both duodenum and ileum of resected and control animals, and there were no effects of resection on tissue radiotracer 65Zn concentrations or specific activities in the mucosal fraction or underlying tissues. Calculations of mucosal entry and exit fluxes per centimeter segment length showed that the major effect of resection was to increase the zinc entry flux at the luminal surface of the mucosa. At the basal surface of the mucosa, both entry and exit fluxes increased.(ABSTRACT TRUNCATED AT 250 WORDS)
Adaptation, Physiological↗
The role of intestinal intubation in obstruction of the small intestine due to carcinoma of the ovary.
A total of 165 episodes of obstruction of the small intestine associated with carcinoma of the ovary were evaluated retrospectively to define the role of intestinal intubation. Patients with prolonged tube suctioning (greater than 48 hours) had a significantly higher operative mortality than patients operated upon immediately without prior intubation or after short term intubation of no longer than 48 hours (p less than 0.05). When controlled for risk factors, such as age, tumor status, ascites and amount and type of prior therapy, the difference between the groups was no longer significant (p greater than 0.1). Another variable of importance was the response to tube suction as documented by serial plain roentgenograms of the abdomen. Prolonged tube suction did not result in increased morbidity compared with short term intestinal intubation (p greater than 0.1) if decompression of the small intestine was accomplished within 48 hours of admission. Nonoperative therapy by intestinal intubation rarely relieves small intestinal obstruction caused by carcinoma of the ovary. It may, however, relieve distension of the small intestine proximal to the obstruction, thus preventing anatomic and metabolic changes that contribute to poor outcome when surgical treatment for relief of the obstruction is delayed.
Aged↗
Effects of artificial ileocolonic sphincter on motility in intestinal remnant following subtotal small intestinal resection in the dog.
We studied the effects of a sphincter substitute on motility in the intestinal remnant following an extensive distal intestinal resection. Two groups of adult dogs were studied; each underwent a 75% resection of the distal small intestine, and in one group a nipple valve was fashioned at the distal end of the remnant. Nutritional status, absorptive function, motility, and transit were studied over a three-month period. While the nipple valve animals had less diarrhea, steatorrhea, and hypoalbuminemia, motor activity and transit were similar in both groups. Thus, in both groups, fasting motor activity was dominated by clusters of phasic pressure activity. (Cluster frequency, per hour, mean +/- SE, resection vs resection with nipple valve: 4.8 +/- 1.05 vs 3.58 +/- 0.54, NS). We conclude that the beneficial effects of a sphincter substitute in ameliorating the short bowel syndrome in this dog model are not related to any modification of the motor response to resection but may simply reflect those of a low-grade mechanical obstruction.
Animals↗
Distribution of E-cadherin and beta-catenin in relation to cell maturation and cell extrusion in rat and mouse small intestines.
In the small intestines, cell renewal from stem cells present in the crypts is balanced by cell extrusion from the tips of the villi. The mechanism by which extrusion occurs is unknown. Recent in vitro data suggested that loss of E-cadherin could contribute to cell extrusion and induction of programmed cell death (PCD) in mouse small intestinal epithelium. We have studied if this also occurs in the intact rodent small intestine. Our results confirm that extruded cells are negative for E-cadherin. However, loss of the E-cadherin-interacting protein beta-catenin preceded both extrusion and loss of E-cadherin. Thus, all extruded cells as well as all cells in the process of extrusion lacked staining for beta-catenin. Moreover, almost 80% of all cells undergoing programmed cell death, as detected by the TUNEL reaction, lacked beta-catenin whereas over 70% of such cells were positive for E-cadherin. However, most cells lacking beta-catenin did not display signs of PCD as detected by the TUNEL method or by staining for active caspase-3. Therefore, these results suggest that loss of beta-catenin precedes the onset of programmed cell death, loss of E-cadherin and extrusion from the villi.
Animals↗
Jejunal brake: inhibition of intestinal transit by fat in the proximal small intestine.
Optimal absorption of fat requires adequate time of contact with the absorptive sites of the small intestine. In order to prevent steatorrhea, intestinal transit must be slowed in response to the fat that has emptied into the small intestine. Intestinal transit is known to be inhibited by fat in the ileum via the ileal brake. This response has suggested that the regulation of intestinal transit is a function of the distal small intestine. However, clinical observations suggest that the ileal brake is not the only control mechanism for intestinal transit. In short bowel patients with resection of the ileum, the proportion of fecal fat recovery remained constant even after the fat intake was increased threefold. In these patients, optimal fat absorption based on the slowing of intestinal transit must have been triggered by an inhibitory mechanism located outside of the distal small intestine. To test the hypothesis that fat in the proximal small intestine inhibited intestinal transit, we compared intestinal transit during perfusion of the proximal half of the small intestine with 0 (buffer only), 15, 30, or 60 mM oleate in dogs equipped with duodenal and mid-intestinal fistula. Intestinal transit across a 150-cm test segment (between fistulas) was measured by counting for the recovery of a radioactive marker in the output of the mid-intestinal fistula during the last 30 min of a 90-min perfusion. We found that oleate inhibited intestinal transit in a load-dependent fashion (P < 0.005). Specifically, while the mean cumulative recovery of the transit marker was 95.5% during buffer perfusion, the recovery decreased when 15 mM (64.3%), 30 mM o(54.7%), or 60 mM oleate (38.7%) was perfused into the proximal half of the small intestine. We conclude that fat in the proximal small intestine inhibits intestinal transit as the jejunal brake.
Animals↗
Radiologic evaluation and staging of small intestine neoplasms.
The small intestine is an uncommon location for neoplasms in either clinical or radiological practice. Because of its anatomic location and morphology, diagnosis of the diseases that affect small intestine pose difficulties. Symptoms are nonspecific and endoscopy is commonly unsatisfactory. Since early and definite diagnosis is crucial for prompt therapy, radiological imaging plays an essential role. Enteroclysis is the primary and effective radiologic modality in the evaluation of small bowel neoplasms. On the other hand, computed tomography should be the complementary radiologic method as well as for staging. In this review, the most common neoplasms of the small intestine and their common radiologic findings have been discussed.
Adenocarcinoma↗
The metabolism of the small intestine. Oxygen uptake and L-lactate production along the length of the small intestine of the rat and guinea pig.
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Animals↗
Catabolism of neurotensin in the epithelial layer of porcine small intestine.
The mammalian small intestine is both a source and a site of degradation of neurotensin. Metabolites produced by incubation of the peptide with dispersed enterocytes from porcine small intestine were isolated by high-performance liquid chromatography and identified by amino-acid analysis. The principal sites of cleavage were at the Tyr-11-Ile-12 bond, generating neurotensin-(1-11), and at the Pro-10-Tyr-11 bond, generating neurotensin-(1-10). The corresponding COOH-terminal fragments, neurotensin-(11-13) and -(12-13) were metabolized further. Formation of neurotensin-(1-11) and -(1-10) was completely inhibited by phosphoramidon (Ki = 6 nM), an inhibitor of endopeptidase 24.11, but not by captopril, an inhibitor of peptidyl dipeptidase A. Incubation of neurotensin with purified endopeptidase 24.11 from pig stomach also resulted in cleavage of the Tyr-11-Ile-12 and Pro-10-Tyr-11 bonds. A minor pathway of cell-surface-mediated degradation was the phosphoramidon-insensitive cleavage of the Tyr-3-Glu-4 bond, generating neurotensin-(1-3) and neurotensin-(4-13). No evidence for specific binding sites (putative receptors) for neurotensin was found either on the intact enterocyte or on vesicles prepared from the basolateral membranes of the cells. Neurotensin-(1-8), the major circulating metabolite, was not formed when neurotensin(1-13) was incubated with cells, but represented a major metabolite (together with neurotensin-(1-10] when neurotensin-(1-11) was used as substrate. The study has shown that degradation of neurotensin in the epithelial layer of the small intestine is mediated principally through the action of endopeptidase 24.11, but this enzyme is probably not responsible for the production of the neurotensin fragments detected in the circulation.
Animals↗
Abnormal breath tests to lactose, fructose and sorbitol in irritable bowel syndrome may be explained by small intestinal bacterial overgrowth.
BACKGROUND: Small intestinal bacterial overgrowth and sugar malabsorption (lactose, fructose, sorbitol) may play a role in irritable bowel syndrome. The lactulose breath test is a reliable and non-invasive test for the diagnosis of small intestinal bacterial overgrowth. The lactose, fructose and sorbitol hydrogen breath tests are widely used to detect specific sugar malabsorption. AIM: To assess the extent to which small intestinal bacterial overgrowth may influence the results of hydrogen sugar breath tests in irritable bowel syndrome patients. METHODS: We enrolled 98 consecutive irritable bowel syndrome patients. All subjects underwent hydrogen lactulose, lactose, fructose and sorbitol hydrogen breath tests. Small intestinal bacterial overgrowth patients were treated with 1-week course of antibiotics. All tests were repeated 1 month after the end of therapy. RESULTS: A positive lactulose breath test was found in 64 of 98 (65%) subjects; these small intestinal bacterial overgrowth patients showed a significantly higher prevalence of positivity to the lactose breath test (P < 0.05), fructose breath test (P < 0.01) and sorbitol breath test (P < 0.01) when compared with the small intestinal bacterial overgrowth-negatives. Small intestinal bacterial overgrowth eradication, as confirmed by negative lactulose breath test, caused a significant reduction in lactose, fructose and sorbitol breath tests positivity (17% vs. 100%, 3% vs. 62%, and 10% vs. 71% respectively: P < 0.0001). CONCLUSIONS: In irritable bowel syndrome patients with small intestinal bacterial overgrowth, sugar breath tests may be falsely abnormal. Eradication of small intestinal bacterial overgrowth normalizes sugar breath tests in the majority of patients. Testing for small intestinal bacterial overgrowth should be performed before other sugar breath tests tests to avoid sugar malabsorption misdiagnosis.
Adult↗
Complete sequences of glucagon-like peptide-1 from human and pig small intestine.
In the small intestine, proglucagon is processed into the previously characterized peptide "glicentin" (proglucagon (PG) 1-69) and two smaller peptides showing about 50% homology with glucagon: glucagon-like peptide-1 and -2. It was assumed that the sites of post-translational cleavage in the small intestine of the proglucagon precursor were determined by pairs of basic amino acid residues flanking the two peptides. Earlier studies have shown that synthetic glucagon-like peptide-1 (GLP-1) synthesized according to the proposed structure (proglucagon 71-108 or because residue 108 is Gly, 72-107 amide) had no physiological effects, whereas a truncated from of GLP-1, corresponding to proglucagon 78-107 amide, strongly stimulated insulin secretion and depressed glucagon secretion. To determine the amino acid sequence of the naturally occurring peptide we isolated GLP-1 from human small intestine by hydrophobic, gel permeation, and reverse-phase high performance liquid chromatography. By analysis of composition and sequence it was determined that the peptide corresponded to PG 78-107. By mass spectrometry the molecular mass was determined to be 3295, corresponding to PG 78-107 amide. Furthermore, mass spectrometry of the methyl-esterified peptide showed an increase in mass compatible with the presence of alpha-carboxyl amidation. Thus, the gut-derived insulinotrophic hormone GLP-1 is shown to be PG 78-107 amide.
Amino Acid Sequence↗
Novel nuclear corticosteroid binding in rat small intestinal epithelia.
When small intestinal epithelial cells are incubated with [(3)H]corticosterone, nuclear binding is displaced neither by aldosterone nor RU-28362, suggesting that [(3)H]corticosterone is binding to a site distinct from mineralocorticoid receptor and glucocorticoid receptor. Saturation and Scatchard analysis of nuclear [(3)H]corticosterone binding demonstrate a single saturable binding site with a relatively low affinity (49 nM) and high capacity (5 fmol/microg DNA). Competitive binding assays indicate that this site has a unique steroid binding specificity, which distinguishes it from other steroid receptors. Steroid specificity of nuclear binding mirrors inhibition of the low 11beta-dehydrogenase activity, suggesting that binding may be to an 11beta-hydroxysteroid dehydrogenase (11betaHSD) isoform, although 11betaHSD1 is not present in small intestinal epithelia and 11betaHSD2 does not colocalize intracellularly with the binding site. In summary, a nuclear [(3)H]corticosterone binding site is present in small intestinal epithelia that is distinct from other steroid receptors and shares steroid specificity characteristics with 11betaHSD2 but is distinguishable from the latter by its distinct intracellular localization.
11-beta-Hydroxysteroid Dehydrogenase Type 1↗
[Clinico-morphologic diagnosis of lesions of the initial portions of the small intestine in peptic ulcer of the stomach and small intestine].
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Adult↗
[Adenoma of the small intestine in a 5-year-old child producing a 7-ringed invagination of a considerable portion of the small intestine].
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Adenoma↗
Protective effect of leptin against ischemia-reperfusion injury in the rat small intestine.
BACKGROUND: The small intestine is extremely sensitive to ischemia-reperfusion (I/R) injury and a range of microcirculatory disturbances which contribute to tissue damage. Previous studies have shown that leptin plays an important physiological role in the microvasculature. The aim of this study was to evaluate the protective effects of leptin in I/R--induced mucosal injury in the small intestine. METHODS: Forty rats were divided into 5 groups (n = 8). Group I was subjected to a sham operation. Following mesenteric ischemia in group II (control); physiologic saline 1 cm3, in group III; leptin 100 microg/kg, and physiologic saline 1 cm3, in group IV; NG-L-arginine methyl ester (L-NAME) 20 mg/kg, and physiologic saline 1 cm3, in group V; leptin 100 microg/kg, L-NAME 20 mg/kg, and physiologic saline 1 cm3 were given intra-peritoneally. In these groups, an I/R procedure was performed by occlusion of the superior mesenteric artery for 45 min followed by 120 min reperfusion. After reperfusion, the small intestines were resected for malondialdehyde (MDA) and nitric oxide (NO) concentration and histopathologic properties. Mucosal lesions were scored between 0 and 5. Tissue MDA and NO concentration and histopathologic grades were compared statistically. RESULTS: Tissue MDA level significantly increased (P < 0.05), tissue NO level significantly decreased in group V animals, compared to group III animals respectively (P < 0.001). Histopathologically, intestinal injury significantly decreased in the leptin treated ischemic group. CONCLUSION: Leptin can be used safely in mesenteric occlusive diseases, since it induces NO formation and release in mesenteric vessels.
Animals↗