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PubMed1977

Intestinal bypass. A comparison between two different bypass operations and resection of the small intestine in rats.

General nutrition, intestinal absorption and liver structure and function were compared in rats subjected to: 1) 90 per cent resection of the small intestine, 2) 90 per cent small intestinal bypass with end-to-side jejunoileostomy (ES bypass), and 3) 90 per cent small intestinal bypass with end-to-end jejuno-ileostomy and anastomosis between the excluded segment and the colon (E-E bypass). The E-E bypass group showed the highest mortality rate and the lowest body weight. In this group the haemoglobin concentration, the faecal fat excretion, and the liver function parameters were more abnormal than in resected rats. Rats with E-S bypass showed results in between the other two groups. In none of the animals was fatty infiltration or cirrhosis of the liver observed. It is concluded that intestinal bypass in rats has a more deleterious effect than resection, and this seems to be more pronounced when the excluded segment is anastomosed to the colon. Factors that might be responsible for this effect are discussed.

Alanine Transaminase↗
PubMed2004

Advanced gastric carcinoma with a complete intestinal metaplasia phenotype associated with early intestinal-type carcinoma.

An unusual case of synchronous gastric carcinomas occurred in a 28-year-old man with a family history of gastric disease. Two tumor foci were identified: a well-differentiated advanced carcinoma with the phenotypic properties of complete intestinal metaplasia and an early intestinal-type carcinoma. Histochemical and immunohistochemical stains to demonstrate complete intestinal metaplasia, ie, Alcian blue pH 2.5/periodic acid-Schiff, high iron diamine/Alcian blue pH 2.5, CD10, and MUC2, were all positive in the advanced adenocarcinoma. Of all markers used, only high iron diamine/Alcian blue pH 2.5 and Alcian blue pH 0.5 were positive in the early carcinoma. In these cases, mistakes frequently are made during examination of endoscopic biopsies. Fortunately, the advanced adenocarcinoma was low grade (the patient has shown no signs of disease at 6 years postsurgery). Histopathologic, histochemical, and immunohistochemical findings suggest that an extensive substrate of complete intestinal metaplasia (corpus) and of complete and incomplete intestinal metaplasia (antrum) can be associated with two independent tumors with different phenotypes.

Adenocarcinoma↗
PubMed1975

Effect of acute intestinal obstruction on the leakage of albumin from blood into the small intestine.

The effect of a simple, low intestinal obstruction has been investigated in dogs on the leakage of 131I-serum albumin from the circulation into the intestine. An increase leakage has been demonstrated. In the distended segment of the intestine above that ligation a significant increase in protein-bound radioactivity, from the normal value of 0.082 plus or minus 0.012 ml/10 cm intestine/hour to 0.276 plus or minus 0.068 ml/10 cm intestine/hour, was obseved which means a more than 3fold increase. The values for albumin leakage did not change in the more proximal segments of the intestine less involved in the distension namely in the duodenum and the jejunum, furthermore in the ileal segment below the ligation. The increase in albumin liadage observed during intestinal obstruction resulted in 33% rise of total catabolism.

Acute Disease↗
PubMed1999

[Apoptosis of small intestinal epithelial cells in small intestinal allograft rejection].

OBJECTIVE: To investigate apoptosis of epithelial cells during small intestinal allograft rejection in rats. METHODS: Heterotopic small intestinal transplantation was performed with inbred rat F344/N (RT1(l)) and inbred rat Wistar/A (RT1-A(k), RT1-E(d)). All recipients were divided into four groups: group I, nonoperative control (Wistar); group II, isograft control (Wistar-->Wistar); group III, allograft (F344-->Wistar); group IV, treatment control [F344-->Wistar + Cyclosporine A (6 mg x kg(-1) x d(-1))]. The grafts were harvested on day 3, 5, 7 after operation. All graft samples were subjected to histological examination and apoptotic cells of graft epithelial cells with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). RESULTS: Histologically mild acute rejection occurred on day 3 after operation in group III, moderate acute rejection on day 5 after operation, severe acute rejection on day 7 after operation. But none of group II had the histological evidence of acute rejection and the histological evidence of group IV indicated that Cyclosporine A could effectively controlled small intestinal acute allograft rejection. The TUNEL showed that the number of apoptotic cells per crypt in group III was significantly higher than that of the other three control groups on day 3 and day 5 after operation (P < 0.01). The epithelial mucosa in group III completely sloughed on day 7 after operation. CONCLUSIONS: Apoptosis plays an important role in small intestinal allograft rejection. Detection of apoptotic cells with TUNEL could be a valuable tool for the diagnosis of small intestinal allograft rejection.

Animals↗
PubMed2002

Ethanol promotes intestinal tumorigenesis in the MIN mouse. Multiple intestinal neoplasia.

Epidemiological studies suggest that alcohol consumption increases the risk of developing colorectal cancer; however, these data are confounded by numerous cosegregating variables. Previous experimental reports with the rodent carcinogen model have also yielded discordant results. To clarify the alcohol-colon cancer relationship, we used the MIN (multiple intestinal neoplasia) mouse, a genetic model of intestinal tumorigenesis. Twenty-four MIN mice were randomized to ethanol supplementation in the drinking water (15% alternating with 20% on a daily basis) or control. Mice were sacrificed after 10 weeks, and the intestinal tumors were scored under magnification. Tissue sections were assessed for apoptosis and cell proliferation rates, along with the presence of the malondialdehyde-acetaldehyde (MAA) adduct, a mutagenic adduct associated with ethanol consumption. Ethanol supplementation resulted in a significant increase in tumor number (135 +/- 35%; P = 0.027 versus control). The induction of tumorigenesis by ethanol was most dramatic in the distal small bowel (167 +/- 56%; P = 0.01). In the uninvolved intestinal mucosa, there was no difference in proliferative or apoptotic indices. Cytoplasmic and nuclear MAA adducts were detected in both ethanol-treated and control mice. We demonstrated that ethanol ingestion increased intestinal tumorigenesis in the MIN mouse model. Furthermore, whereas mechanisms remain incompletely elucidated, our data implicate formation of MAA adducts. This report provides further support that ethanol consumption is a risk factor for colorectal cancer.

Abnormalities, Multiple↗
PubMed1991

[Intraoperative intubation of the small intestine in surgery of mechanical intestinal obstruction. Experience with a method of intraoperative and postoperative maintenance in mechanical obstruction using a long multi-pierced tube applied intraoperatively].

The Authors describe their experience from 1986 to 1990 of intraoperative intubation of the small intestine to obtain intra- and post-operative decompression of intestinal loops and for prevention or postoperative adhesions in intestinal obstruction case. Two methods are reported; one using the ready-made long intestinal "Baker" tube, and another consisting of using a self-made tube with available materials. Enumeration of cases is reported, and the lack of complications from the use of the method is stressed. The good result in the prognosis of obstructive intestinal disease is also stressed.

Adult↗
PubMed1986

Light microscopic immunocytochemical localization of hepatic and intestinal types of fatty acid-binding proteins in rat small intestine.

Monospecific antisera to purified hepatic fatty acid-binding protein (hFABP) and gut fatty acid-binding protein (gFABP) have been used to localize these two proteins in the small intestine of fed rats at the light microscopic level. Pieces of duodenum, jejunum, and ileum were removed from 4-, 10-, 20-, 22-, and 60-day-old Sprague-Dawley rats. Both cryostat and paraffin sections were studied for the presence of hFABP or gFABP by the avidin-biotin immunoperoxidase method. Slides were graded blind for the intensity of staining. Despite the structural and immunological differences between these two proteins, we showed no major differences between their staining patterns or their staining intensity throughout the intestine during postnatal development. The staining for both fatty acid-binding proteins was cytoplasmic. No brush border staining was found. Staining was more intense in the proximal rather than distal intestine, in the villus rather than crypt cells, and in the apex rather than the base of intestinal cells. Shifts in staining patterns, and staining intensity occurring during development may be related to variations in dietary fat intake, rates of cell proliferation, intestinal anatomy, and mechanisms for fat absorption.

Animals↗
PubMed1985

[Small intestine perfusion. The authors' own method for the simultaneous performance of biopsy and perfusion of the human small intestine].

The analysis of advantages and disadvantages of the technique and principles of the methods of small intestinal perfusion, used by various authors in the studies on resorption processes, provided grounds the authors to develop their own method. The system for infusion and aspiration by a combined probe is described. Details about the composition of perfusion solution, the technique of the study and calculation of resorption rate are reported. The advantages of the method are as follows: simultaneous performance of small intestinal glucose perfusion and biopsy of small intestine, good tolerance by the patients and availability of the elements needed for the construction of the probe and system for infusion and aspiration. The mean glucose resorption rate was 814,07 mumol/min/30 cm in 9 subjects with no small intestinal diseases and with normal histomorphological picture of small intestinal mucosa.

Biopsy, Needle↗
PubMed1982

Alpha-2 adrenergic inhibition of intestinal secretion induced by prostaglandin E1, vasoactive intestinal peptide and dibutyryl cyclic AMP in rat jejunum.

Effects of alpha adrenergic agents on intestinal secretion induced by prostaglandin E1 (PGE1), vasoactive intestinal peptide (VIP) and dibutyryl cyclic AMP (Bt2cAMP) were investigated in rat jejunum in vivo. Oxymetazoline and clonidine were more potent than epinephrine in inhibiting the PGE1-induced secretion. Methoxamine failed to inhibit the PGE1-induced secretion even with a 100-fold higher dose than that of clonidine. A high dose (1 mumol/kg) of oxymetazoline not only inhibited the PGE1- induced secretion but also enhanced net fluid absorption. Yohimbine reversed the inhibitory effect of clonidine, whereas phenoxybenzamine did not. These antagonists per se did not produce any effects on PGE1-induced secretion. Clonidine inhibited the intestinal secretion induced by VIP or Bt2cAMP, whereas methoxamine did not. The inhibitory effect of clonidine was reversed by yohimbine. Phenoxybenzamine per se inhibited intestinal secretion induced by either VIP or Bt2cAMP. Clonidine did not produce any significant effects on PGE1- augmented cAMP levels in jejunal mucosa in vivo. These results suggest that stimulation of alpha-2 adrenoceptors in rat jejunal mucosa inhibits some mechanisms distal to cAMP generation and in turn results in the inhibition of net water intestinal secretion. These findings also raise the question of general validity of a hypothesis that alpha-2 adrenoceptors regulate cellular functions through the inhibition of adenylate cyclase activity.

Adrenergic alpha-Agonists↗
PubMed1995

N-ethyl-N-nitrosourea treatment of multiple intestinal neoplasia (Min) mice: age-related effects on the formation of intestinal adenomas, cystic crypts, and epidermoid cysts.

The timing of intestinal tumor initiation in B6-Min/+ mice has been examined by treating mice at 5-35 days of age with a single i.p. injection of the direct-acting alkylating agent N-ethyl-N-nitrosourea (ENU). Treatment of Min/+ mice at 5-14 days of age resulted in a 3.8-fold increase in intestinal tumor multiplicity over untreated mice. Mice treated at 20-35 days of age showed only a 1.6-fold increase in tumor number. These results, in conjunction with examination of tumor multiplicities of untreated Min/+ mice as a function of age, suggest that the majority of intestinal tumors in Min/+ mice are initiated relatively early in life. Min/+ mice treated with ENU also showed an increase in the number of cystic intestinal crypts. However, the relationship between age at ENU treatment and cystic crypt multiplicity was distinct from that seen for intestinal adenomas. Mice treated at 5-9 days of age showed only a 1.9-fold increase in cystic crypts over untreated animals. By contrast, the increase in average cystic crypt multiplicity for mice treated at 10-35 days of age was 4.5-fold. In addition, 60% of Min/+ mice treated with ENU before 25 days of age developed epidermoid cysts, an extracolonic manifestation commonly associated with familial adenomatous polyposis in humans.

Adenoma↗
PubMed1975

[Effect of intestinal flora and diet on rat intestinal pool and fecal excretion of bile salts].

Comparative studies between groups of rats which differ by the microbial flora of their gastrointestinal tract, the weight of their caecum and the diet on which they are fed allow the following conclusions: 1. Caecal enlargement is, on the one hand, mainly responsible for the increased intestinal pool of bile salts in the intestine of germ-free rats and on the other has little action on the decrease of their fecal excretion. 2. Other than for intestinal flora, diet modifies intestinal pool and fecal excretion of bile salts. Fecal excretion mainly depends on diet cholesterol content. Intestinal pool size mainly depends on dietary factors which are different from cholesterol.

Animals↗
PubMed1977

[Electron microscopic study of the small intestine in intestinal lymphangiectasia and constrictive pericarditis (author's transl)].

Electron microscopic study of the small intestine in cases of intestinal lymphangiectasia and in cases of constrictive pericarditis was performed. This study revealed that numerous chylomicron-like particles are present in the lymphatic lumina, in the extracellular spaces of the lamina propria, and within the interepithelial spaces between the absorptive cells. Presence of chylomicron-like particles in the intestinal lumen suggested possibility of passage of these substances into the intestinal tract through the interepithelial spaces. Similar findings to those as seen in intestinal lymphangiectasia were observed in constrictive pericarditis. A few pseudopode-like cytoplasmic projections of the undifferentiated crypt cells were noted. Other mechanisms of enteric protein loss are postulated.

Chylomicrons↗
PubMed1997

[The importance of tapering the intestines in congenital intestinal atresia].

Extensive intestinal resections in inborn intestinal atresias are the second most frequent cause of the short gut syndrome. Because treatment of this condition is so far minimal, prevention is of fundamental importance. One possible approach is tapering of the gut, i.e. longitudinal antimesenterial resection of the gut. At the Clinic of Paediatric Surgery in 1991-1995 30 patients with inborn atresias of the gut were operated (17 atresias of the duodenum, 11 atresias of the small intestine, 2 atresias of the large intestine). Six patients (20%) died. In 2 patients (one girl with atresia of the colon and one boy with atresia of the jejunum) developed dilatation of the gut orally from the site of resection of the atresia and a chronic subileous condition. Instead of resection of the dilated portion the gut was modelled by tapering. In both children the passage improved and the children thrive. Based on data in the literature and their own experience the authors assume that tapering of the gut should supplement primarily high jejunal atresia, apple peel syndrome and extensive dilatation of the jejunum. Tapering cannot be used above the aganglionic portion of the intestine.

Female↗
PubMed1989

Decreased binding of vasoactive intestinal peptide to intestinal epithelial cells from hypothyroid rats.

The binding of vasoactive intestinal peptide (VIP) and stimulation of adenylate cyclase by VIP were studied in intestinal epithelial cells during hypothyroidism. Experimental hypothyroidism was induced in rats by the administration of KC10(4). The binding capacity, but not the affinity, of VIP receptors decreased in the hypothyroid rats. Besides, the stimulation of cyclic AMP production by VIP was also diminished in cells from hypothyroid rats. These observations indicate a decrease of the responsiveness of intestinal epithelial cells to VIP in the hypothyroid status, suggesting a role of the peptide in the pathophysiologic mechanism of intestinal manifestations during hypothyroidism.

Animals↗
PubMed2005

Antisecretory actions of a novel vasoactive intestinal polypeptide (VIP) antagonist in human and rat small intestine.

Vasoactive intestinal peptide (VIP) has been demonstrated in intestinal mucosal neurones and elicits chloride secretion from enterocytes. These findings have led to the proposal that VIP is a secretomotor neurotransmitter. Confirmation of such a role may now be possible with the development of PG 97-269, a high-affinity, selective antagonist of VIP type 1 (VPAC1) receptor, which is expressed by gut epithelial cells. We have evaluated the VIP antagonism and antisecretory potential of this novel compound using in vitro and in vivo models of intestinal secretion. Monolayers of the human colonic cell line (T84) and muscle-stripped preparations of rat jejunum and human ileum were set up in Ussing chambers for recording of transepithelial resistance and short-circuit current. Ussing chambers were modified to allow electrical stimulation of mucosal neurones. Effects of PG 97-269 on enterotoxin-induced secretion were investigated in perfused rat jejunum in vivo. PG 97-269 competitively antagonised VIP in T84 monolayers. In rat jejunum and human ileum, responses to VIP were inhibited as were responses of rat jejunum to electrical stimulation of mucosal neurons. In perfused rat jejunum, PG 97-269 abolished the effects of VIP on fluid and electrolyte transport and attenuated cholera toxin and Escherichia coli heat labile toxin-induced net fluid and electrolyte secretion. PG 97-269 is a competitive antagonist of enterocyte VIP receptors and effectively inhibits responses of rat and human intestinal mucosa to VIP. Antagonism of secretory responses to electrical stimulation of mucosal neurons and lumenal application of enterotoxins imply a secretory role for VIP in these processes.

Animals↗
PubMed1985

Effect of resection of small intestine on the interaction of vasoactive intestinal peptide with rat colonic epithelial cells.

Vasoactive intestinal peptide (VIP) receptors and VIP-dependent cyclic AMP production were studied in rat colonic epithelial cells 3 days after a 60% resection of the small intestine. Basal cyclic AMP levels were similar in both control and resected animals. The potency, but not the efficiency, of the peptide on the stimulation of cyclic AMP production was diminished in cells from resected rats. Accordingly, the affinity of VIP receptors, but not the binding capacity, decreased as a consequence of the loss of a part of the small intestinal mucosa. These observations are consistent with the known inhibitory role of cyclic AMP on cell proliferation in colonic epithelium and other tissues and suggest a participation of VIP acting through the cyclic nucleotide in the compensatory hyperproliferative response of the colon following massive resection of the small intestine.

Animals↗
PubMed1999

Human intestinal mast cells produce IL-5 in vitro upon IgE receptor cross-linking and in vivo in the course of intestinal inflammatory disease.

IL-5, known to be produced by T lymphocytes and eosinophils, is a key regulator of intestinal diseases such as parasitosis or eosinophilic gastroenteritis. Here we examined if mast cells contribute to the IL-5 production in human intestinal mucosa. The number of IL-5-positive lamina propria cells was substantially higher in patients with intestinal inflammatory diseases (5.3 +/- 4.6%, n = 17) compared to healthy controls (0.5 +/- 0.9%, n = 8, p < 0.01). In patients, the IL-5-positive cells were eosinophils (70 +/- 13%) and mast cells (29 +/- 14%), whereas in controls all IL-5-positive cells were eosinophils. IL-5-positive T cells were not detected, likely because they do not store IL-5. In vitro studies with isolated human intestinal mast cells and eosinophils showed that mast cells do not produce IL-5 constitutively, but release high amounts of IL-5 (315 +/- 115 pg/10(6) cells) following IgE receptor cross-linking, compared to activated eosinophils (24 +/- 5 pg/10(6) cells). Inhibitor studies suggest a regulation of IL-5 production at the transcriptional level. In conclusion our data demonstrate that activated mast cells are a potent source of IL-5 in the human intestinal mucosa.

Adult↗
PubMed1997

Expression of OCI-5/glypican 3 during intestinal morphogenesis: regulation by cell shape in intestinal epithelial cells.

OCI-5, the rat homologue of human glypican 3 (GPC3), is believed to be involved in morphogenesis and growth control during development. The finding that GPC3 is mutated in patients with the Simpson-Golabi-Behmel overgrowth syndrome is consistent with this idea. In this report, using RNA in situ hybridization, expression of OCI-5 in the developing intestine is detected in both endoderm- and mesenchyme-derived cells in a phased manner related to age and proximal/distal position. To investigate the mechanism of its regulation during intestinal development, OCI-5 expression was studied in the primitive rat intestinal epithelial cell line IEC-18. The expression of the OCI-5 transcript is increased in IEC-18 cells at confluence, in low calcium media, and during spheroid culture, all conditions which result in the cells acquiring a more rounded cell shape. In contrast, cytoskeletal disruption with colchicine causes cells to flatten and spread and abolishes both the confluence- and the low calcium-dependent induction of OCI-5. Treatment with vanadate, a phosphatase inhibitor, causes cells to acquire a spindle-shaped morphology and prevents OCI-5 induction in all situations. Nuclear run-on analysis demonstrates that the rate of OCI-5 transcription is increased at confluence, in low calcium media, and during spheroid culture of IEC-18, and decreased by treatment of cells with colchicine. Together, these data suggest that OCI-5 expression is regulated in IEC-18 by cell shape. The pattern of expression of OCI-5 in the developing intestine is consistent with it playing a role in epithelial-mesenchymal interactions during intestinal morphogenesis, when cell shape changes are likely to occur.

Animals↗