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At least 739 records · Page 41Linked to original sources
PubMed1988

[Modelling and simulation of urea balance in a rat model on the condition of large intestine infusion analogous to the ultrafiltrate as a contribution to the development of an implantable intestinal hybrid kidney].

The urea kinetics in blood plasma is discussed for the animal model in rats in the development conception of an implantable artificial kidney, in which the filtration process is received energetically endogenically by a technical hemofilter whereas the ultrafiltrate procedure takes place by intestinal reabsorption and elimination of the end-products. The underlying monocompartment model contains the elements plasma, hemofilter, intestine including their urea turnover rates. Further on a special model conception is developed for the animal experimental designation of the selective urea reflecting power of the intestinal mucosa. The hemofilter-intestine-hybrid kidney-system has chanced to be in order if the experimentally ascertained quantities of the preliminary experiments will be inserted simultaneously for essential parameters in the model experiment.

Animals↗
PubMed1987

[Diffuse intestinal polyangiomatosis as a cause of recurrent intestinal hemorrhage. Report of an unusual case].

We observed a 38-year-old Italian male with recurrent intestinal bleeding and consecutive iron-deficient anemia. For search of the source of bleeding intensive clinical, endoscopic and radiological investigations had been performed. Multiple malformations of superior mesenteric artery with abnormal vascularisation of jejunum and ileum were established angiographically. In addition the lumen of small bowel loops was dilated and enlarged mucosa folds were found. Because of a prominent vascularized area in the cecum a resection of the right hemicolon had been performed with consecutive death of the patient. The post mortem investigation revealed dilated mesenteric arteries, multiple cavernous hemangiomata in the mesenterium, in the wall of the small bowel and solitary in the large bowel. Additionally angiodysplasias, phlebectasias, lymphangiectasias, and lymphangiomata in the large bowel and in the mesenterium were found. "Diffuse intestinal polyangiomatosis" is the proposed term of the syndrome consisting of recurrent intestinal bleeding and multiple intestinal vascular malformations.

Adult↗
PubMed1986

Intestinal calcium and phosphate transport and intestinal alkaline phosphatase.

The aim of the study was to investigate the link, if any, between alkaline phosphatase activity and intestinal calcium and phosphate transport using the hypophysectomized (HX) rat model. Ionic transport was evaluated by the in situ ligated loop technique. Hypophysectomy (HX) resulted in a decrease in both duodenal and jejunal alkaline phosphatase activity but did not alter the active transport of calcium and phosphate. Vitamin D depletion (-D), suppressed intestinal transport in the HX rat without altering alkaline phosphatase activity. Repletion of 1,25(OH)2D3 in the -DHX rat resulted in an increase in active transport of calcium and phosphate without altering the alkaline phosphatase activity. Thus, using the HX animal model, we were able to differentiate intestinal alkaline phosphatase activity from the overall intestinal transport of calcium and phosphate.

Alkaline Phosphatase↗
PubMed1995

Intestinal failure and intestinal transplantation: new therapy for individuals sustaining large losses of bowel: a review.

Intestinal failure is a concept developed to define the situation wherein either severe primary gastrointestinal disease or a surgically induced short bowel syndrome exists and prevents an adequate oral intake of nutrients such that parenteral nutrition is required. Typically, because of disease associated problems, total parenteral nutrition is required in most cases of intestinal failure. The major cause of intestinal failure in both adults and children is surgical resection resulting in a short bowel syndrome. The clinical signs and symptoms of a short bowel syndrome include any combination of the following: intractable diarrhea, steatorrhea, failure to thrive, acidosis, dehydration, trace element deficiency syndromes, hypoproteinemia, hypovitaminosis, and anemia. It is often difficult to predict at the time of a bowel resection whether or not a short bowel syndrome will occur postoperatively. This is the case because any of a number of confounding problems such as (a) difficulty in precisely estimating the length of the remaining small bowel at the time of the operation, (b) the presence of disease in the residual small bowel that can produce further shortening or impair residual intestinal function, and (c) the presence or absence of the ileal cecal valve, which can be critical in determining the adaptability of the residual bowel.

Graft Survival↗
PubMed1995

Comparative study of the enzyme activities of Borrelia burgdorferi and other non-intestinal and intestinal spirochaetes.

Comparative analysis of the enzymatic profiles of 58 spirochaetal isolates clearly differentiated borrelias from leptospires, serpulinas and a treponeme. Strains of both Borrelia burgdorferi and Borrelia hermsii characteristically produced significant amounts of leucine arylamidase. This enzyme activity was not unique to borrelias but was also detected amongst pathogenic and non-pathogenic leptospira serovars. This fact, however, did not hamper a correct differentiation of borrelias from these spirochaetes, because leptospires possessed unique enzyme profiles. The API ZYM system could not differentiate the human strains of B. burgdorferi from those isolated from ticks, or from B. hermsii. Treponema phagedenis could be differentiated from all the other spirochaetes by the production of alpha-fucosidase. Our results confirm and extend previous studies indicating that human and animal intestinal spirochaetes have many common enzyme activities. All strains produced reactions of maximum intensity when tested for the presence of beta-galactosidase activity. However the avian strains lacked esterase (C4) which was present in human and swine intestinal spirochaetes. All strains of Serpulina hyodysenteriae, and Serpulina innocens as well as the human intestinal spirochaete strain HRM-14 showed alpha and beta glucosidase activity. Both enzyme activities were absent or insignificant in most other intestinal spirochaetes examined: 25 different human strains, non-pathogenic swine strain M1 and the avian strain 4742. However, swine strain LL3 and avian strain 1380 showed some beta-glucosidase activity.

Animals↗
PubMed1993

Biochemical detection of small intestinal allograft rejection by elevated circulating levels of serum intestinal fatty acid binding protein.

BACKGROUND: Intestinal fatty acid binding protein (I-FABP) was investigated as a serum marker for acute intestinal allograft rejection. Its behavior was compared with that of another putative marker of intestinal damage, hexosaminidase. METHODS: Transplants were performed in three groups of rats: group 1, Lewis to Lewis; group 2, ACI to Lewis, no immunosuppression; and group 3, ACI to Lewis with cyclosporine given on posttransplant days 0 through 5. Daily serum I-FABP and hexosaminidase levels were quantitated and serial graft biopsy specimens were obtained. RESULTS: Serum I-FABP levels fell to 20 ng/ml or less in all animals between posttransplant days 3 and 4. In group 1, I-FABP levels remained at baseline throughout the experiment. In group 2, I-FABP levels rose dramatically on either day 6 or 7 and declined to baseline within 4 days of the peak. On the day that I-FABP levels increased, findings of biopsy specimens were consistent with early rejection. In group 3 the rise in serum I-FABP levels was delayed 2 to 10 days. Hexosaminidase did not correlate with rejection. CONCLUSIONS: Serum I-FABP content correlated with early histologic manifestations of rejection. Hexosaminidase was insensitive as a marker in this model. I-FABP, which has a human analog, has potential as a biochemical marker for early intestinal allograft rejection.

Animals↗
PubMed1997

CD4+ T cell down-regulation in human intestinal mucosa: evidence for intestinal tolerance to luminal bacterial antigens.

T cells from the intestinal mucosal proliferate poorly in vitro, and the contribution of Ag-specific recognition to this hyporesponsiveness is unclear, since the Ag repertoire of intestinal mucosal T cells is unknown. In this study, T cell proliferation in response to Ag-prepulsed autologous peripheral blood-derived APC was examined. Whereas T cells from peripheral blood proliferated to inner membrane and cytoplasmic Escherichia coli proteins, T cells from intestinal mucosa responded only to purified component Ags of these proteins and not to their combination. This suggests that the lack of proliferation in response to these Ags presented as a mixture is not due to the absence of E. coli-specific T cells in the mucosa, but, rather, to down-regulation after T cell recognition. Down-regulation was assayed by measuring the inhibition of autologous peripheral blood T cell proliferation in response to Ag-prepulsed APC. Coculture with leukocytes from intestinal mucosa and not from mesenteric lymph nodes, inhibited autologous peripheral blood T cell proliferation in response to E. coli proteins, but not to tetanus toxoid, PHA, or IL-2. Inhibition was independent of cell contact, provided APC were available to the mucosal cell population, and was reversible by neutralization of IL-10 or TGF-beta with mAb or depletion of mucosal CD4+ T cells. Taken together, the data suggest that mucosal T cell unresponsiveness to luminal Ags is mediated by production of inhibitory cytokines after specific Ag recognition by CD4+ T cells.

Aged↗
PubMed2000

Inhibition of intestinal tumors by curcumin is associated with changes in the intestinal immune cell profile.

BACKGROUND: The C57BL/6J-Min/+ (Min/+) mouse bears a germline mutation in Apc and is therefore a model for familial adenomatous polyposis and sporadic colorectal cancer. Min/+ intestinal mucosa exhibits a marked tendency for spontaneous adenoma formation. Curcumin is a phenolic antioxidant known for its antitumor and immune modulatory functions in vitro. Curcumin prevents adenoma formation in Min/+ mice, through a mechanism that may be related to its immunomodulatory properties. MATERIALS AND METHODS: To study the relationship between intestinal immunity and curcumin-induced antitumor response, we used immunohistochemistry to characterize the effect of curcumin treatment on resident intestinal immune effector cells in Min/+ mice. RESULTS/CONCLUSION: These results show that mucosal CD4(+) T cells and B cells increase in animals treated with curcumin, suggesting that curcumin modulates lymphocyte-mediated immune functions.

Adenomatous Polyposis Coli Protein↗
PubMed1989

Autonomic innervation of the intestine from a baby with megacystis microcolon intestinal hypoperistalsis syndrome: I. Immunohistochemical study.

A typical case of megacystis microcolon intestinal hypoperistalsis syndrome (MMIHS) is reported. The patient, an infant girl, was fed only by total intravenous nutrition and is now 3 years old. The distribution of several gut peptides was examined in the resected small intestine using an immunohistochemical method. Vasoactive intestinal polypeptide (VIP) and peptide histidine methionine (PHM)-containing nerve fibers were decreased; however, substance P- and leucine enkephalin (Leu-ENK)-containing fibers were increased. The imbalance between several kinds of gut peptides might be one the causes of aperistalsis in MMIHS. This is the first report about the gut peptides of MMIHS.

Autonomic Nervous System↗
PubMed2002

New therapeutic approach in the management of intestinal disease: probiotics in intestinal disease in paediatric age.

Current evidence supports the view that oral administration of probiotics may be of therapeutic usefulness in several clinical disorders by reestablishing normal flora in the gastrointestinal tract. These entities include inflammatory and infectious diseases of the gut as well as extraintestinal disorders (such as atopic eczema) in which a defective intestinal permeability plays a role. The probiotic effects are attributed to restoration to normal of increased intestinal permeability, unbalanced gut microecology, improved immunological gut barrier function, downregulation of the intestinal inflammatory responses with reduced generation of proinflammatory cytokines. Entities for which the impact of probiotic administration can be considered as proven are Rotavirus diarrhoea, Clostridium difficile diarrhoea, post-antibiotic diarrhoea, allergic diseases. On the other hand, entities for which administration of probiotics is considered under investigation are inflammatory bowel disease, necrotizing enterocolitis, cystic fibrosis, small bowel bacterial contamination, functional gastrointestinal disorders. The value of probiotics as therapy for a variety of gastrointestinal disorders in childhood still needs to be investigated in detail, through well controlled and rigorous studies, including a placebo group and strict criteria of randomisation. Much work needs to be done in this area by clearly defining indications, delivery system, costs, safety long-term effects.

Child↗
PubMed1975

Substrate interactions on the intestinal mucosa: a concept for the regulation of intestinal digestion.

1. The hydrolysis of glycyl-L-leucine, glycyl-L-tyrosine, tributyrin, sucrose, maltose, soluble starch and alpha- and beta-glycerophosphates by everted segments of rat intestine was estimated separately or in combination. 2. A comparative study showed significant interaction between different substrates which affected their digestion. 3. Two types of interaction were identified: products of hydrolysis (1) affected the hydrolysis of homologous substances, e.g. methionine and alanine inhibited glycyl-L-leucine hydrolysis, maltose reduced glucoamylase (alpha-1,4-glucan glucohydrolase; EC 3-2-1-3) activity (intracatenary interactions); (2) interfered with the hydrolysis of a different group of substances, e.g. tributyrin inhibited dipeptidase (glycyl-L-leucine hydrolase; EC 3-4-3-2) and alkaline phosphatase (EC 3-1-3-1), glycyl-L-leucine interfered with the activity of the latter enzyme (intercatenary interactions). 4. Mechanisms of interactions were suggested by the results of a comparison of the extent of inhibition or activation of two enzymes (glycyl-L-leucine hydrolase and alkaline phosphatase) in situ in everted intestinal segments or after solubilization with papain or Triton X-100, and different treatments known to affect allosteric sites of these enzymes. 5. Tributyrin and dipeptides were found to act on alkaline phosphatase as allosteric regulators. A discontinuity of the Arrhenius plot suggested the existence of different enzyme conformations which were re-arranged by tributyrin. 6. Substrate interactions in digestion were found in adult rat, cat, rabbit and hen. Substantial differences were found between classes (Aves and Mammalia), orders (rodents, lagomorphs and carnivores) and between age-groups within an animal strain (in this instance, for the rat). 7. These interactions are thought to be involved in the co-ordination of digestion with intestinal absorption and to regulate the time and site of subsequent hydrolysis.

Alkaline Phosphatase↗
PubMed1978

The effects of small intestinal colonization by fecal and colonic bacteria on intestinal function in rats.

The effects of colonic and fecal bacterial proliferation on jejunal function were studied in normal rats and in low-germ rats after intraperitoneal injections of mecamylamine HCl. Jejunal bacteriology, bile salts, ultrastructure, and transport capacity were assessed. Normal rats given mecamylamine for 3 days had increased anaerobic bacteria in the intestinal fluid, and had high concentrations of deconjugated bile salts in the intraluminal contents. Jejunal bacteria were lodged between microvilli without penetrating the cell cytoplasm. However, there was focal cellular damage, including fused microvilli, dilated endoplasmic reticulum, and secondary lysosomes. In the mecamylamine treated normal rats intestinal glucose transport was reduced with an alteration compatible with noncompetitive inhibition. The absorption rates of galactose, fructose, 3-0-methyl-D-glucose, tyrosine, Na, and K were also decreased. In contrast, low-germ mecamylamine-treated rats showed no evidence of either increased anaerobic bacterial proliferation or deconjugation of bile salts, and had none of the fine structural alterations seen in regularly raised rats. Also, the transport of carbohydrates was unaltered. The findings suggest that non-invasive enteric proliferation of colonic and fecal bacterial anaerobes in rats may be associated with deconjugation of bile salts, ultrastructural alterations of the intestinal epithelial cells, and a diminished jejunal transport capacity of carbohydrates and other solutes.

Anaerobiosis↗
PubMed2004

Intestinal adaptation occurs independently of parenteral long-chain triacylglycerol and with no change in intestinal eicosanoids after mid-small bowel resection in rats.

The role of enteral or parenteral long-chain triacylglycerol (LCT) in the complex process of intestinal adaptation is poorly defined and may involve alterations in eicosanoid synthesis. Our objective was to determine whether provision of parenteral LCT stimulates eicosanoid synthesis and resection-induced intestinal adaptation. We assessed small bowel structural adaptation, the fatty acid profiles of liver, plasma and jejunal mucosa, and the profile of 11 eicosanoids derived from (n-6) PUFA of the jejunal mucosa in rats maintained with total parenteral nutrition (TPN) with 0 or 32% of nonprotein energy from Intralipid for 7 d after mid-small bowel resection or transection control surgery. There was no evidence of biochemical essential fatty acid (EFA) deficiency in the absence of parenteral fat. Resection-induced gut growth occurred independently of parenteral LCT based on significant mucosal hyperplasia in the jejunum and ileum. The mucosal profile of linoleic acid in the total lipid extract of jejunum increased with the presence of parenteral LCT, but decreased with resection without differences in arachidonic acid. There were no differences in the jejunal profile of 11 (n-6)-derived eicosanoids among the four TPN groups as determined by tandem MS. In summary, small bowel resection-induced adaptation occurs independently of parenteral LCT, and fat-free TPN without EFA deficiency does not alter the profile of jejunal (n-6)-derived eicosanoids. Thus, parenteral administration of LCT does not appear to alter jejunal eicosanoid synthesis nor is it beneficial in stimulating intestinal adaptation.

Adaptation, Physiological↗
PubMedDate not supplied

Disaccharidase activities and intestinal absorption in infants with congenital intestinal obstruction.

The results of studies on disaccharidase activities and on intestinal absorption in cases of complete and incomplete congenital small bowel obstruction are presented. Assays of the activities of maltase, isomaltase, sucrase, trehalase, and lactase have been performed on biopsy specimens taken at the time of surgery. In specimens taken from above the site of obstruction, the activities are reduced for all disaccharidases, and are particularly low for trehalase and lactase. There was no difference between the cases with complete and incomplete obstruction. Distal to a complete obstruction, trehalase and lactase were reduced, whereas in cases of incomplete obstruction, the activities of all disaccharidases were within what is considered normal in the reference material. Two months after surgery, the disaccharidase activities were found to be normal. One month after surgery, the absorption of glucose and vitamin A was markedly impaired in cases with complete obstruction, whereas that of D-xylose was not significantly reduced from normal. In cases with incomplete obstruction, the results did not differ from those found in normal infants. The fact that failure to thrive is common during the first months after birth in patients with congenital intestinal atresia, even when surgery is successful, may be explained by deficient intestinal absorption, particularly in patients with complete obstruction.

Body Weight↗
PubMed1986

A cytokinetic study of small-intestinal and colonic mucosa after resection of 70% of the small intestine.

Pulse-labelling with tritiated thymidine and a fraction of labelled mitoses experiments have been performed in order to investigate the proliferative changes induced at various sites in the hyperplastic small-intestinal mucosa of rats previously subjected to resection of 70% of the small intestine. Proliferative activity in the colon was also studied. In the distal ileum there is a significant reduction in cell cycle time (Tc) of cells at all levels within the crypt and the growth fraction falls. In the jejunum and proximal ileum the crypts contain an increased number of proliferating cells, but as the size of the maturation zone is also increased, there is no significant alteration in the relative number of proliferating cells per crypt. Nor does the distribution of proliferating cells in these crypts seem to alter. There is no general reduction in Tc at these sites, but there does appear to be a significant reduction in Tc on the part of the cells in the stem-cell zone at the crypt base. In neither proximal nor distal colon was there any significant proliferative change apparent after small-intestinal resection.

Animals↗
PubMed1988

The effect of splanchnic nerve stimulation and neuropeptide Y on cholera secretion and release of vasoactive intestinal polypeptide in the feline small intestine.

The effect of sympathetic nerve stimulation and intra-arterial infusion of neuropeptide Y (NPY) on net fluid secretion and release of vasoactive intestinal polypeptide (VIP) was studied in the cat small intestine during a secretion due to cholera toxin. Activation of the splanchnic nerves (4 Hz, 5 ms, 5 V) decreased net fluid secretion to 57 +/- 10% of control. Concomitantly, the release of VIP was reduced to less than 50%. Furthermore, close i.a. infusion of NPY (estimated increase in plasma concentration 75 nmol l-1) reduced the net fluid secretion and VIP release to 27 +/- 5 and 28 +/- 4% of the pre-stimulatory value. The correlation between the decrease in net fluid secretion and reduction in VIP release showed a strong positive correlation (r = 0.83). These results strongly indicate that the antisecretory effect of sympathetic nerve stimulation during cholera diarrhoea is mediated by inhibition of secretory VIP neurons in the intestinal mucosa. A similar mechanism is also proposed for the intravascularly administered NPY.

Animals↗
PubMed2003

In vivo modulation of intestinal CYP3A metabolism by P-glycoprotein: studies using the rat single-pass intestinal perfusion model.

P-Glycoprotein (P-gp) has been hypothesized to modulate intestinal drug metabolism by increasing the exposure of drug to intracellular CYP3A through repeated cycles of drug absorption and efflux. The rat single-pass intestinal perfusion model was used to study this interplay in vivo. N-Methyl piperazine-Phe-homoPhe-vinylsulfone phenyl (K77), a peptidomimetic cysteine protease inhibitor (CYP3A/P-gp substrate), and midazolam (CYP3A substrate) were each perfused through a segment of rat ileum alone and with the P-gp inhibitor N-(4-[2-(1,2,3,4-tetrahydro-6,7-dimethoxy-2-isoquinolinyl)-ethyl]-phenyl)-9,10-dihydro-5-methoxy-9-oxo-4-acridine carboxamine (GG918). Samples were obtained continuously from the outlet perfusate and the mesenteric vein at 5-min intervals for 40 to 60 min. The parent drug and two main metabolites of K77 (N-desmethyl and N-oxide) and midazolam (1-OH and 4-OH) were quantitated by liquid chromatography/mass spectrometry. K77 appearance in the mesenteric blood (P(blood) = 5 +/- 3 x 10(-6) cm/s) was increased 3-fold with GG918, whereas midazolam permeability (P(blood) = 1.1 +/- 0.3 x 10(-4) cm/s) was unchanged by GG918. K77 metabolites were preferentially excreted into the lumen, 4-OH midazolam was found equally in lumen and blood, and 1-OH was mainly excreted into blood. The extent of metabolism was estimated by calculating the fraction metabolized = 1 - P(blood)/P(lumen) and the extraction ratio (ER) determined from the direct measurement of known metabolites as ER = sum metabolites(all)/(sum metabolites(all) + drug in blood). When P-gp was inhibited, the fraction metabolized for K77 was decreased (95 to 85%) and the ER tended toward a decrease, whereas no differences in either parameter were observed for midazolam (not a P-gp substrate). These data support a role for P-gp in modulating the extent of intestinal metabolism in vivo by controlling drug access to the enzyme.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1983

Studies of intestinal lymphoid tissue. VI--Proliferative response of small intestinal epithelial lymphocytes distinguishes gluten- from non-gluten-induced enteropathy.

Several diseases of the small intestine, including gluten-sensitivity, present with malabsorption and a "flat" mucosa. Determination of the mitotic index of epithelial lymphocytes provides a simple, objective method of assessing, and thus of predicting, whether a flat mucosa is due to gluten-sensitivity (index greater than 0.2%), or not (index less than 0.2%). The use of this index in circumstances especially likely to cause diagnostic confusion--for example, intestinal lymphoma; Crohn's jejunitis of immunodeficiency--is illustrated in this paper. Of seven cases, five (two primary lymphoma, three immunodeficiency) had been treated with a gluten-free diet without benefit; a mitotic index performed on the initial biopsy in each of these patients could have predicted from the outset that none was gluten-sensitive. Of the remaining two cases, determination of the mitotic index on the biopsy initially obtained from a man with severe hypogammaglobulinaemia would have indicated that he was also gluten-sensitive. Empirical use of a gluten-free diet was avoided in the other patient (with flat small intestinal mucosa and low mitotic index) in whom the diagnosis was ultimately shown to be due to Crohn's disease of jejunum.

Adolescent↗