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Intestinal adaptation in atrophic rat ileum is accompanied by supersensitivity to vasoactive intestinal peptide, pituitary adenylate cyclase-activating peptide and nitric oxide.

BACKGROUND: Intestinal inactivity leads to atrophic changes and concomitant alterations in the expression of neurotransmitters in the enteric nervous system. In atrophic rat ileum neurones expressing vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating peptide (PACAP) decrease in number while nitric oxide synthase (NOS) expressing neurones increase. Since little is known about functional changes accompanying intestinal atrophy the aim of the present study was to investigate relaxatory responses to VIP, PACAP-27 and nitric oxide (NO) in longitudinal smooth muscle from atrophic rat ileum. METHODS: To create a dysfunctional (atrophic) intestine, the distal 10 cm of rat ileum was surgically bypassed. In vitro experiments were carried out on longitudinal muscle strips from rat ileum having been sham-operated, one week or four weeks bypassed. RESULTS: The amplitudes of the relaxatory responses to PACAP-27, VIP and the NO-donor S-nitroso-N-acetylpenicillamine (SNAP), but not forskolin, were significantly increased in the one-week bypassed ileum. In the four-weeks bypassed ileum the VIP, PACAP-27, SNAP and forskolin evoked relaxations were of the same magnitude as those of the sham-operated. The augmented responses to both VIP and PACAP-27 could be blocked by pre-treatment with apamin while N(G)-nitro-L-arginine methyl ester (L-NAME) and tetrodotoxin were ineffective. In contrast to sham-operated and four-weeks bypassed ileum, cross-desensitization between VIP and PACAP-27 was noted after one week of bypass. CONCLUSION: Intestinal adaptation after bypassing the distal ileum of the rat includes a transient supersensitivity of the longitudinal muscle to the NO donor SNAP, VIP and PACAP-27. These augmented relaxatory responses may contribute to the hypomotility noted in inactive intestine.

Adaptation, Physiological↗

[Effect of shenfu injection on recovery of intestinal function, cellular immunity, serum interleukin-2 and tumor necrosis factor-alpha in children with intestinal obstruction after operation].

OBJECTIVE: To observe the effect of Shenfu injection (SFI) on recovery of intestinal function, T-lymphocyte subsets (CD4, CD8 and CD4/CD8), interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) in children with intestinal obstruction after surgical operation. METHODS: Ninety-eight children suffering from intestinal obstruction after emergent surgical operation were divided into the SFI group (n = 50, treated with SFI after operation) and the control group (n = 48, treated with surgical operation alone). The intestinal function recovery rate (IFRR), T-lymphocyte subsets, serum levels of IL-2 and TNF-alpha in them were observed. RESULTS: After being treated for 7 days, the IFRR in the SFI group was 84.0%, which was significantly higher than that in the control group (62.5%, P < 0.05). CD4, CD4/CD8 levels increased in the SFI group after treatment (P < 0.05), while in the control group, CD8 increased significantly after treatment (P < 0.05) and higher than that in SFI group (P < 0.01). IL-2 level was much higher in the SFI group after treatment than that in the control group (P < 0.05). TNF-alpha level significantly lowered in both groups (P < 0.01), and the level in the SFI group was lower than that in the control group (P < 0.05). CONCLUSION: SFI could promote the recovery of intestinal function, improve and regulate the immune function of the children after operation for intestinal obstruction.

CD4-CD8 Ratio↗

Carbohydrate differentiation antigens of murine T cells: expression on intestinal lymphocytes and intestinal epithelium.

Carbohydrate differentiation antigens (CT antigens) which previously had been shown to be associated with cytotoxic T cells were found at high levels on intestinal intraepithelial lymphocytes (IEL) and on the intestinal epithelium. Histological examination of intestinal sections demonstrated that the CT1 MAb defined epitopes on IEL and on epithelial cells located in the base of the villi crypts. The CT2 MAb reacted with IEL but also bound to the majority of cells in the intestinal epithelium. When isolated intestinal cell populations were analyzed by flow cytometry, two major size classes of cells were evident. The smaller cells, corresponding to lymphocytes, were primarily Lyt-2+, with a high proportion expressing CT antigens. Another differentiation antigen defined by the MAb J11d was absent from IEL, indicating that those IEL of T cell origin are likely to be mature because thymocytes, but not peripheral T cells, express the J11d antigen. Two-color fluorescence analysis indicated that the CT determinants were present on the Thy-1+, Lyt-2+, and the Thy-1-, Lyt-2+ subsets of IEL. However, the small percentage of L3T4+ IEL were CT-, further supporting our previous demonstration of a correlation between CT expression and Lyt-2 expression. Interesting phenotypic characteristics of IEL other than CT antigen expression were also detected. IEL did not express the MEL-14 lymphocyte homing receptor, and the cell surface level of LFA-1 was significantly lower than that of other peripheral lymphocytes. It was also shown that a small percentage of IEL express a T cell receptor allotypic marker, indicating that at least some of the cells are mature in terms of T cell receptor gene rearrangements. The large intestinal cells, although CT+, were not hematopoietic in origin because they were T200- and were shown by using chimeric mice not to be bone marrow-derived. In contrast to previously reported results, the cytotoxic activity of IEL was negligible with detectable lysis against NK-sensitive cells and other tumor cells, being observed in only one of seven experiments. Thus, the expression of the CT determinants was not indicative of cytotoxic ability, as previously suggested. The presence of specific carbohydrate residues on the cell surface of a subset of lymphocytes in an anatomically distinct immune compartment suggests that a unique differentiation pathway is followed by these cells.

Animals↗

Respiratory activity of various parts of the small intestine in fasted and fed animals. Part II. Respiratory activity of the small intestine in guinea pigs.

The aim of this work was to investigate the respiratory activity of three parts of the small intestine: duodenum, jejunum and ileum in guinea pigs, to compare the intensity of oxygen consumption by these parts in hungry and fed animals, and to find possible differences in the intensity of intestinal respiration between guinea pigs and rats. In guinea pigs the intensity of respiration of intestinal homogenates was nearly twice smaller than in rats. similarly, however, as in rats intestinal homogenates of guinea pigs had greater respiration intensity after feeding than while the animals were fasting. The metabolic gradient in the small intestine of guinea pigs was somewhat different, the intensity of respiration was highest in the jejunum, in the duodenum it was slightly lower or equal to that in the ileum it was the lowest. The intensity of mitochondrial respiration was similar in guinea pigs as in rats, and the metabolic gradient in mitochondrial respiration was also similar in three studied parts of the intestine. The effects of fasting and feeding were, however, different than in homogenates. the mitochondria of fed animals consumed less oxygen than those of fasting animals. These changes in respiration were not connected with any changes in the amounts of mitochondrial protein since they were similar in fasting and in fed animals.

Animals↗

[New computerized tomography sign of intestinal infarction: isolated pneumoretroperitoneum or associated with pneumoperitoneum or late findings of intestinal infarction].

INTRODUCTION: We retrospectively reviewed the CT findings of the acute abdomen patients examined in the last two years to investigate the frequency of a new CT sign of intestinal infarction, the pneumoretroperitoneum, and its association with other CT findings highly suggestive of this condition. MATERIAL AND METHODS: The CT findings of 60 patients with diagnostic confirmation of intestinal infarction were retrospectively reviewed. CT was performed without (no. = 55) and with (no. = 5) oral administration of contrast material and without (no. = 3) and with (no. = 57) the i.v. injection of nonionic contrast agents in repeated 50 mL boluses. To assess the specificity of this sign, we selected a control group of 400 patients submitted to CT for acute abdomen, but not blunt trauma; 19 of these patients had pneumoretroperitoneum. RESULTS: Pneumoperitoneum was found in five patients with intestinal infarction; it was an isolated sign in two cases and it was associated with few small perihepatic air bubbles in one case. Finally, it was associated with highly suggestive findings of late intestinal infarction in the other two cases. All cases of pneumoretroperitoneum in the control group had been correctly referred to other diseases by previous plain film and/or CT findings and surgery and/or endoscopy confirmed this diagnosis. DISCUSSION AND CONCLUSIONS: Pneumoretroperitoneum has been described as a complication of different benign or severe disorders; prompt recognition of its origin is essential since surgical and/or septic conditions may be involved. However, if the patient's history is negative for abdominal trauma, gastroduodenal ulcer or sepsis, pneumoretroperitoneum is generally cured with conservative treatment. Intestinal infarction or severe ischemia, a usually surgical conditions, should be considered among the different causes of pneumoretroperitoneum alone or associated with pneumoperitoneum or with highly suggestive late findings of infarction such as portal venous gas or pneumatosis intestinalis. This sign had a non-negligible incidence in intestinal infarction in our review (8.5%), but it should be known of and sought with specific window setting to enhance gas depiction on CT images to avoid false negatives.

Aged↗

Isolated crypts form spheres prior to full intestinal differentiation when grown as xenografts: an in vivo model for the study of intestinal differentiation and crypt neogenesis, and for the abnormal crypt architecture of juvenile polyposis coli.

We describe a model system in which single crypts, isolated from newborn rats, were embedded in a type I collagen gel and subcutaneously grafted to the flanks of nude mice, whereupon they underwent full intestinal morphogenesis. Small fragments of small intestine and colon were incubated with the divalent cation chelator EDTA, resulting in the release of crypts and villi. Released crypts were then suspended sparsely in type I collagen gel. Segments of gel containing a single crypt were grafted subcutaneously into a nude mouse. Grafts were harvested at weekly intervals. By 2 days, the mouth of the crypts had joined to seal the crypt and, within 1 week, the structure ballooned to form a spherical cystic structure lined by flattened epithelial cells showing no evidence of cytodifferentiation. After 2 weeks, host stromal cells had invaded the collagen and settled around this spherical crypt. At points where stromal cells appeared in contact with the crypt, the epithelium exhibited a more columnar phenotype. By 4 weeks, the 'crypt sphere' was surrounded by stroma expressing alpha-smooth muscle actin and, at this time, multiple buds appeared that gave rise to new crypts. By 5 weeks, villi had formed and cell lineages associated with the small intestine and colon were present; the original single crypt had transformed into a functional intestinal unit. Therefore, we have shown that a single crypt has the potential to grow, give rise to other crypts and dependent structures such as villi. This model has considerable potential for use in gene transfer experiments in the study of intestinal differentiation, and for the analysis of crypt neogenesis via crypt fission. Moreover, the appearances showed a close resemblance to those seen in juvenile polyposis syndrome (JPS), where the budding and fission of single crypts isolated by stromal overgrowth offers an alternative explanation for the histogenesis of JPS.

Adenomatous Polyposis Coli↗

Phytolacca acinosa Roxb. induces intestinal toxicity through the histamine-MLCK-tight junction axis: Integrated evidence from proteomics, metabolomics, intestinal organoids and epithelial barrier validation.

Phytolacca acinosa Roxb. (PR) is a saponin-rich medicinal plant associated with gastrointestinal toxicity, but the mechanisms underlying PR-induced intestinal barrier injury remain unclear. In this study, raw PR extract was analytically characterized by UPLC-ZenoTOF-MS/MS, confirming triterpenoid saponins as the predominant constituents. C57BL/6&#x202f;J mice were orally exposed to characterized PR extract (1.20 or 12.0&#x202f;g/kg for 5&#x202f;h), and Caco-2 cells and mouse intestinal organoids were used to assess epithelial toxicity and barrier disruption. Histopathology, ELISA, FITC-dextran permeability assays, immunofluorescence, CCK-8, LDH release, western blotting, DIA-based proteomics and untargeted metabolomics were integrated to define toxicological mechanisms. PR induced dose-dependent intestinal inflammation and barrier dysfunction, with the ileum as the most sensitive target. PR increased serum DAO and D-lactate and intestinal TNF-&#x3b1; and IL-1&#x3b2;, disrupted organoid morphology, enhanced epithelial permeability, and reduced ZO-1 expression. Proteomics revealed changes in inflammatory, lipid-metabolic, cytoskeletal and tight-junction pathways, including upregulation of MLCK3 and phospholipase-related proteins and downregulation of ZO-1 and ZO-2. Metabolomics identified histidine metabolism disturbance and histamine accumulation. Integrated multi-omics and pharmacological validation indicated that histamine activated the PLC/IP&#x2083;/Ca&#xb2;&#x207a;/CaM/MLCK cascade, promoting MLC phosphorylation, tight-junction disassembly and epithelial leakiness. MLCK inhibition partially restored ZO-1/ZO-2 expression and attenuated PR-induced epithelial injury. These findings identify the histamine-MLCK-tight junction axis as a key mechanism of PR-induced intestinal toxicity and support hazard identification of saponin-rich PR exposure.

Animals↗

Hypersensitivity to ovalbumin induces chronic intestinal dysmotility and increases the number of intestinal mast cells.

Undiagnosed food allergies have been proposed as possible causes of promoting and perpetuating irritable bowel syndrome . Our aim was to find out if sensitization could induce chronic functional motor disturbances in the intestine and the mechanisms implicated. Rats were sensitized to ovalbumin (OVA) following three hypersensitivity induction protocols, two parenteral and one oral. Rat mast cell protease II (RMCP II) release in response to OVA challenge and immunoglobulin E (IgE) concentration were measured in serum. At least 1 week after challenge, small intestinal motility was evaluated using strain gauges. Intestinal tissue samples from orally sensitized rats were checked for in vitro stimulation with OVA. Mucosal mast cells were counted from duodenum sections. All sensitized rats showed intestinal hypermotility. Only rats sensitized by parenteral procedure showed an increase in RMCP II after OVA challenge in serum. IgEs increased only in the Bordetella pertussis sensitized group. Small intestine sections from orally sensitized rats released more RMCP II than sections from control rats. All sensitized rats showed an increase in the number of mucosal mast cells in duodenum. In conclusion, hypersensitivity to food proteins induces chronic motor alteration that persists long after antigen challenge and an excited/activated state of sensitized mucosal mast cells.

Animals↗

Vasoactive intestinal polypeptide and gastrin-releasing peptide attenuate hepatic microvasculatory disturbances following intestinal ischemia and reperfusion.

BACKGROUND/AIMS: In addition to the primarily affected small bowel, intestinal ischemia and reperfusion (IIR) also leads to a marked decrease in hepatic microcirculation. The aim was to determine the potentially protective effect of the vasoactive hormones vasoactive intestinal polypeptide (VIP) and gastrin-releasing peptide (GRP) on hepatic microcirculation following IIR. METHODS: Using a rat model, three animal groups were subjected to 40 min of intestinal ischemia, two of which were infused with either VIP or GRP (n = 12 each). Following reperfusion, hepatic intravital microscopy was performed. Portal venous perfusion, activities of serum glutamate pyruvate transaminase and alkaline phosphatase, mucosal injury in the small intestine and the expression of antioxidant enzymes glutathione peroxidase, copper-zinc-superoxide dismutase (Cu-Zn-SOD), glutathione reductase and catalase (CAT) in the liver were investigated. RESULTS: Infusion of either VIP or GRP improved hepatic microcirculation and bile flow when compared with the untreated IIR group. VIP and GRP increased portal venous blood flow during reperfusion. VIP reduced the extent of mucosal damage resulting from IIR. GRP caused a decrease in expression of CAT and Cu-Zn-SOD, whereas VIP simply reduced CAT expression. CONCLUSION: This study indicates that vasoactive hormones may attenuate intestinal and hepatic injuries and circulatory disturbances following IIR.

Animals↗

[Can intestinal transplantation constitute treatment for intestinal failure?].

The management of patients with intestinal failure has benefited from progress in parenteral nutrition (PN), especially home-based parental nutrition. Intestinal transplantation is now possible and in some conditions, constitutes the logical treatment option. Since 1985, more than 300 small-bowel grafts have been performed, involving the isolated small bowel with or without the colon (45%), the liver + small bowel (40%) or several organs (15%). 2/3 of recipients were under 20 years of age, and indications were short-bowel syndrome (64%), severe intractable diarrhea (13%), abdominal cancer (13%), or chronic intestinal pseudo-obstruction syndrome (8%). 51% of patients survived > 2 years after the graft. Patient and graft survival depends on the type of immunosuppression, i.e. Cyclosporine or FK 506. The results must be interpreted carefully as they represent the first experience in numerous centers using different immuno-suppressive protocols, without any randomization. The results from the largest of these centers more closely reflect the current situation and may exceed a 70% 2-year survival rate. Functional grafts lead to gastrointestinal autonomy (weaning of PN) while maintaining satisfactory nutritional status and normal growth in childhood. Intestinal transplantation is theoretically indicated for all patients permanently or persistently dependent on PN. However, as PN is generally well tolerated, even for long periods, each indication for transplantation must be carefully weighed up in terms of the iatrogenic risk and quality of life. When PN has reached its limits, especially those associated with vascular, infectious, hepatic or metabolic complications, intestinal transplantation must be undertaken. Transplantation of the small bowel alone remains the first option, as combined liver-small bowel grafting is only indicated in case of life-threatening progressive cirrhogenic liver disease.

Adolescent↗

[An experimental assessment of methods for applying intestinal sutures in intestinal obstruction].

The results of various methods used in applying intestinal sutures in obturation were studied. Three series of experiments were conducted on 30 dogs--resection of the intestine after obstruction with the formation of anastomoses by means of double-row suture (Albert--Shmiden--Lambert) in the first series (10 dogs), by a single-row suture after V. M. Mateshchuk [correction of Mateshuku] in the second series, and bu a single-row stretching suture suggested by the author in the third series. The postoperative complications and the parameters of physical airtightness of the intestinal anastomosis were studied in dynamics in the experimental animals. The results of the study: incompetence of the anastomosis sutures in the first series 6, in the second 4, and in the third series one. Adhesions occurred in all animals of the first and second series and in 2 of the third series. Six dogs of the first series died, 4 of the second, and one of the third. Study of the dynamics of the results showed a direct connection of the complications with the parameters of the physical airtightness of the anastomosis, and the last-named with the method of the intestinal suture. Relatively better results were noted in formation of the anastomosis by means of our suggested stretshing continuous suture passed through the serous, muscular, and submucous coats of the intestine.

Anastomosis, Surgical↗

[Endométriosis of the small intestine. Report of 4 new cases of stenosis of the small intestine (author's transl)].

The authors report 4 new cases of stenosis of the small intestine of endometrial origin. They emphasize the rareness of these stenosing forms which in most recent series intervened in 1 case of endometriosis out of 1,000 (Martinbeau). They consider the various clinical presentations encountered, asymptomatic forms discovered by chance, forms associated with suggestive gynecological disorders, chronic stenosis of the small intestine or presentation with intestinal obstruction. They consider the diagnostic difficulty in the isolated forms (2 cases) in the absence of pelvi-genital lesions. Among the positive factors, they consider the recrudescence during theperiods of the digestive signs, the macroscopic appearance of the lesions and, above all, the mucosal integrity noted on opening the specimen after intestinal resection. Finally, they consider certain special problems, that of bi-polar intestinal involvement with double localisation, involving the ileum and the recto-sigmoid areas.

Adult↗

[Activity of small intestine alkaline phosphatase in the feces in chronic intestinal diseases].

In comparison to normal controls (n = 71) the activity of intestinal alkaline phosphatase in feces is reduced in chronic bowel disease using an immunoprecipitation method: patients with Crohns disease (n = 40) or inactive ulcerative colitis (n = 29) demonstrate small changes of fecal intestinal alkaline phosphate activity in comparison to normal controls. Intestinal alkaline phosphatase is reduced in patients with active ulcerative colitis (n = 11) to 50%, in patients with uraemic enteropathy (n = 18) to 30% and in patients with coeliac disease (n = 14) to 20% of the activity observed in normal controls. During cytostatic treatment of malignant tumors, fecal intestinal alkaline phosphatase activity increases as a sign of toxic damage of the intestinal mucosa.

Alkaline Phosphatase↗

Effects of heparin, venous strangulation obstruction of the small intestine, and reperfusion of the small intestine on plasma diamine oxidase activity in horses.

Diamine oxidase (DAO), an enzyme of small intestinal origin, is released from mucosal storage sites by IV administration of heparin, to yield the plasma postheparin DAO (PHD) curve. The PHD curve is diminished when mucosal surface area is lost, and baseline (without heparin) plasma DAO activity increases when mucosal storage sites are damaged. Plasma DAO activity was measured after 2 doses of heparin were administered IV in healthy, conscious horses. In anesthetized horses, the PHD curve was studied: during sham small intestinal surgery, and during venous strangulation obstruction (VSO) of the distal 50% of the small intestine. In a third group of anesthetized horses, baseline plasma DAO activity (without heparin) was measured during VSO of the distal 50% of the small intestine for 90 minutes, followed by reperfusion for 90 minutes. Postheparin plasma DAO curves in conscious horses were similar to those reported in other species. Horses with VSO had a similar PHD curve as did sham-operated controls at all times, except at 15 minutes, when plasma DAO activity was significantly (P < 0.05) greater in the VSO group. Horses with VSO and reperfusion had no change in baseline plasma DAO activity throughout the study. Peritoneal fluid DAO activity remained low throughout the study, but increased slightly in horses with VSO that received heparin, possibly because of DAO from extravasated blood in the peritoneal fluid. Results indicated that the plasma DAO response to IV administered heparin in horses is similar to that in other mammals, but, unlike other species, baseline and postheparin DAO activities did not change as expected after small intestinal vascular obstruction and mucosal injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Amine Oxidase (Copper-Containing)↗

Diffuse lymphoplasmacytic infiltration of the small intestine with damage to nerve plexus. A cause of intestinal pseudo-obstruction.

We describe the clinicopathologic characteristics of three patients with chronic intestinal pseudo-obstruction and malabsorption. The patients were young women (average age, 25 years) who presented with abdominal pain, nausea, vomiting, diarrhea, and weight loss that led to extreme inanition and death in two patients despite multiple treatment schemes. The evolution of the process averaged 8 years. No case manifested evidence of malignant lymphoproliferative progression. Histologically, a diffuse lymphoplasmacytic infiltrate that affected all the layers of the intestinal wall was observed in full-thickness biopsy specimens. The proliferating lymphocytes were small and mixed with mature plasma cells that proved to be polyclonal on immunohistochemical analysis. An outstanding finding in all three cases was extensive damage to submucosal and myenteric nerve plexus associated with a lymphoid infiltrate. Quantification of the myenteric plexus by using immunohistochemical and morphometric techniques also revealed a marked reduction in their number. We concluded that diffuse lymphoplasmacytic infiltration of the small intestine associated with damage to the intestinal nerve plexus constitutes a specific disorder that is different from other diseases that produce intestinal pseudo-obstruction.

Adult↗

Regional specialization of the mucosal immune system. Intraepithelial lymphocytes of the large intestine have a different phenotype and function than those of the small intestine.

Intraepithelial lymphocytes (IEL) are found in both the small and the large intestine. We demonstrate that there are a number of striking phenotypic and functional differences between the two populations of IEL isolated from mice. In the large intestine, the majority of IEL express the alpha beta TCR, and among these TCR-alpha beta+ lymphocytes, CD4+ cells are as prevalent as CD8+ cells. In contrast, in the small intestine, most of the TCR-alpha beta+ IEL express CD8, and an increased percentage of cells express TCR-gamma delta. In addition, most TCR-gamma delta+ IEL isolated from the large intestine (LI-IEL) are CD4- CD8- cells, as compared to TCR-gamma delta+ IEL isolated from the small intestine (SI-IEL), which are predominantly CD8+. Furthermore, CD2 and the lymph node homing receptor, L-selectin, are expressed by most LI-IEL but not by SI-IEL. Furthermore, LI-IEL have much less cytolytic activity than SI-IEL. These data suggest that LI-IEL are a distinct population of lymphocytes that may have a different immunologic role than that of SI-IEL.

Animals↗

Pancreatic extract and the intestinal uptake of vitamin B12. I. Effect on the intestinal epithelium and the vitamin B12-intrinsic factor complex.

Pancreatic extract (PE) reduced the uptake of rat intrinsic factor (IF)-bound 57CoB12 by perfused rat intestinal segments (p is less than 0.02) as well as by isolated rat intestinal brush borders (p is less than 0.01). The inhibition was concentration-dependent. Preincubation of the brush borders with PE recular weight of the 57CoB12-IF complex, as well as the uptake of the complex by isolated intestinal brush borders, was unchanged after prolonged preincubation with PE. PE also inhibited the uptake of glucose by perfused intestinal segments (p is less than 0.01), but the morphology and idsaccharidase activity (p is greater than 0.5) of the intestinaleptihelium was unaltered. The results indicate that the inhibition may be due to interaction between the intestinal epithelium and PE.

Animals↗

Intestinal hypertrophy after small intestinal bypass in the rat. Studies on methods and reversibility of changes.

A jejuno-ileostomy was created in rats, bupassing 85--90% of the small intestine, by means of a self-emptying blind loop. Control animals were subjected to laparotomy and suture-making of vie intestinal segments. At the end of the experiments, intestinal wet and dry weight and villus height were determined in the five different segments of the small intestine taken from both experimental and control animals. After 2 weeks, a significant hypertrophy occurred in the functioning part of the small intestine of the shunt-operated animals, while an atrophy occurred in the blind loop. In a shunt-operated group of animals, the normal anatomy was re-established after 2 weeks and the animals were sacrificed 4 weeks later and compared with (a) control animals, (b) shunt-operated animals. In the re-operated animals, the hypertrophic changes disappeared and, except for the increased wet weight of one jejunal and one ileal segment (p less than 0.05), there were no significant differences in comparison with the control animals. The villus height did not differ significantly from that of the control animals, except for the second jejunal segment, whicntestine of the rat, developing during the 2 weeks after establishment of a jejuno-ileal bypass, are reversible within 4 weeks.

Animals↗