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PubMed2003

Hypertonic saline resuscitation reduces apoptosis and tissue damage of the small intestine in a mouse model of hemorrhagic shock.

The effect of hypertonic saline resuscitation on intestinal damage and the incidence of apoptosis after hemorrhagic shock were investigated. After anesthesia, male BALB/c mice weighing 24-34 g were hemorrhaged to the mean arterial pressure of 40 +/- 5 mmHg for 90 min. Animals were randomly assigned to four groups: 1) resuscitation with 4 mL/kg of 7.5% NaCl (hypertonic saline; HS) + shed blood (SB); 2) resuscitation with two times the volume of shed blood of lactated Ringer's solution (2LR) + SB; 3) sham (catheter only); or 4) control (no treatment). Intestinal damage was graded based on the extent of the vacuolation at the basal area of the intestinal villi. Apoptosis of the small intestines was examined with the terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphosphate nick-end labeling method and with DNA laddering. Caspase-3 activation, heat shock protein (HSP) 70, and HSP40 were assessed by western blotting. Apoptosis of the small intestine and intestinal damage were significantly lower (P < 0.01) in the HS+SB group compared with the 2LR+SB group 2 h and 6 h after hemorrhagic shock and resuscitation, respectively. This corresponded with more DNA fragmentation in the small intestine of the 2LR+SB group compared with the HS+SB group 2 h after hemorrhage and resuscitation. In addition, we observed less caspase-3 activation in the small intestine of the HS+SB group compared with the 2LR+SB group at 2 h after resuscitation. The content of HSP40 and HSP70 in the HS+SB group was similar to that in controls, but slightly decreased in the 2LR+SB group. HS resuscitation reduced intestinal damage and apoptosis after hemorrhagic shock, suggesting that HS resuscitation may improve the outcome after hemorrhagic shock by reducing apoptosis and damage to the small intestine.

Animals↗
PubMed1979

Anion-stimulated ATPase activity of brush border from rat small intestine.

Differential centrifugation of rat small intestinal homogenates produced a crude brush border (BB) fraction that was enriched 15-fold for the marker enzymes, alkaline phosphatase and sucrase; contamination with mitochondrial enzymes, monoamine oxidase and succinate dehydrogenase, was minimal. ATP hydrolysis by this BB fraction was stimulated by addition of several anions to the incubation medium: HCO3 and Cl were equally effective in this regard, with NO3, NO2, SO4, and acetate being less stimulatory. SCN and CNO inhibited ATPase activity, whereas the divalent anion SO3 was stimulatory at low concentrations (less than 25 mM) but inhibitory at 100 mM. Maximum anion stimulation was observed at a Mg concentration of 0.5 mM, and pH optimum was 8.5. Kinetic analysis showed that HCO3 increased the Vmax without altering the Km for ATP; the Ka for this effect of HCO3 was 35 mM. This enzyme activity was completely inhibited by 20 mM L-phenylalanine, 10 mM L-cysteine, and 3 mM EDTA, compounds that also inhibited intestinal alkaline phosphatase. These results demonstrate the presence of anion-stimulated ATPase activity in rat small intestinal brush border and suggest that this activity may be related to intestinal alkaline phosphatase. The role of this enzyme in intestinal transport is not known, but could relate to the regulation of intestinal absorption and secretion.

Adenosine Triphosphatases↗
PubMed1999

[Perforation of the small intestine].

BACKGROUND: Small bowel perforation is a major problem in abdominal typhi disease, but is seldom observed in Italy, as Salmonella typhi infections are rare in this Nation. The cause of perforation varies greatly. The reported mortality is high and varies from 23 up to 42%. A retrospective study has been performed in order to find how to improve the outcome. METHODS: A series spanning 10 years is reviewed, from January 1, 1987 to December 31, 1997, comprising 60 patients with small bowel perforation, operated in a urgency setting in the Operating Room of the Emergency Department of the Molinette Hospital in Torino. Resection and primary anastomosis were utilized in 33 patients, 27 underwent oversewing. In 3 patients a colostomy was felt necessary because of a concomitant damage of the colon. RESULTS: No leakages occurred. Hospital stay varies from 1 day to 76 days (24 days mean). Mortality is consistent with literature: 20 patients (33%) but the cause is related to the primary diseases of the patients. Delay in diagnosis did not affect the patient's outcome. CONCLUSIONS: In conclusion, it is confirmed the one-time surgery as the choice treatment in small bowel perforations from causes other then S. typhi infection. Mortality is not directly related to the consequences of surgical repair.

Abdominal Injuries↗
PubMed1987

A study of the histopathogenesis of carcinoid tumors of the small intestine and appendix.

A specimen from the small intestine with multiple (three) classic carcinoid tumors and one appendiceal carcinoid tumor displaying argentaffinity, argyrophilia (Grimelius stain), and serotonin and neuron specific enolase immunoreactivity was examined by light microscopy with regard to the tumor cell histopathogenesis. The smallest tumor (diameter 0.5 cm) from the small intestine was cut into 512 and the appendiceal tumor into 511 serial sections, which were stained with the argyrophil technique. In the small intestine an increased number of endocrine cells and small proliferating aggregates of endocrine cells were observed among nonendocrine enterocytes in the crypts of Lieberkühn. They seemed to grow initially inside the crypts and to later infiltrate through the basement membrane into the lamina propria of the mucosa. This finding suggests that classic carcinoid tumors of the small intestine develop from mucosal endocrine (enterochromaffin) cells. Since proliferating argentaffin cells were also seen in the mucosal crypts in one of the other two carcinoid tumors (2 cm in diameter) in the same intestine specimen, it is suggested that when multiple carcinoid tumors occur in the small intestine they arise from multiple sites. There was no apparent connection between the mucosal crypts and the carcinoid tumor of the appendix. Thus in this particular case, the appendiceal carcinoid tumor did not appear to derive from the mucosal endocrine cells but from the subepithelial endocrine cells that are present in the lamina propria and submucosa of the appendix wall. Supporting this view is the fact that S-100 protein immunoreactive cells are found both in close relation to subepithelial endocrine cells and as an integral component of appendiceal carcinoid tumors.

Appendiceal Neoplasms↗
PubMed1988

Physiological and pharmacological regulation of small intestinal cholesterol synthesis.

1. The small intestine is an important site of cholesterol synthesis in the body and at least in experimental animals, it also contributes to the circulating plasma pool of cholesterol. 2. Studies on synthesis regulation have been partly contradictory but it is now concluded that the cellular cholesterol balance is the basic regulatory factor of intestinal cholesterol synthesis. However, the balance is affected differently in various specialized cells and parts of the small intestine. 3. Most data on synthesis regulation are derived from experimental animals but the few human studies suggest that similar regulatory factors function in man, too.

Animals↗
PubMed2000

Phagocytic and intestinal endothelial and epithelial barrier function during the early stage of small intestinal ischemia and reperfusion injury.

The effects of intestinal ischemia and reperfusion (I/R) on small intestinal mucosal endothelial and epithelial barrier integrity and phagocytic function were assessed in rats subjected to 20- or 40-min mesenteric ischemia and a 3-h reperfusion. The results showed that human serum albumin (125I-HSA) flux through the endothelial layer to the interstitial space increased as did 125I-HSA clearance from blood to the gut lumen and 131I-HSA flux from the gut lumen to the interstitial space in rats with I/R. E. coli adhering to microvilli, invading and passing into the microvessels, were noted on the small intestinal mucosa in animals subjected to 40-min ischemia and a 3-h reperfusion. Phagocytic function increased, especially in the small intestinal wall, lungs, liver, and spleen in the groups with I/R, correlating with the length of ischemia. The results imply that both endothelial and epithelial barrier integrity is impaired in the early phase after I/R and that the epithelial barrier more effectively restricts macromolecular leakage compared with the endothelial barrier. I/R impairs the intestinal barrier not only by causing tissue hypoxia but also by activating the phagocytic system and aggravating barrier damage, which finally may result in bacterial translocation and remote organ dysfunction.

Animals↗
PubMedDate not supplied

T cell progenitors in the murine small intestine.

Lymphocytes in the murine small intestine epithelium are known to have a high proportion of extrathymic T cells. To explore the possibility that small intestine intraepithelial lymphocytes (IELs) are derived from T cell progenitors present within the intestine, intestine-derived cells with characteristics of early-stage T cell precursors were studied for their ability to regenerate IEL T cell populations following transfer into irradiated recipient mice. Cells within this population lacked markers of mature T cells but expressed heat-stable antigen, the c-kit receptor for stem cell factor, and/or the pre-T cell alpha gene. Upon adoptive transfer, donor cells preferentially homed to the intestine and did not repopulate the thymus or extraintestinal peripheral lymphoid tissues. IELs derived from the donor precursor pool included both (alpha beta and gamma delta T subsets and consisted of phenotypically heterogeneous cell populations defined by CD4 and CD8. These findings provide evidence that T cell progenitors located in the intestinal mucosa are the likely source of most intestinal IELs.

Animals↗
PubMed2005

[Small intestinal bacterial overgrowth. An update].

Small intestinal bacterial overgrowth (SIBO) is characterized by nutrient malabsorption, associated with an excessive number of bacteria in the proximal small intestine. Unfortunately, the diagnosis of bacterial overgrowth presents several difficulties and limitations, and as yet there is not a widespread agreement on the best diagnostic test. SIBO occurs when there are alterations in intestinal anatomy, gastrointestinal motility, or a lack of gastric acid secretion. The true association between SIBO and irritable bowel syndrome and celiac disease remains uncertain. The treatment usually consists in the eradication of bacterial overgrowth with repeated courses of antimicrobials, nutritional support and when it is possible, the correction of underlying predisposing conditions.

Anti-Bacterial Agents↗
PubMed1998

Liver damage in human small intestinal bacterial overgrowth.

OBJECTIVE: Some rodent strains with experimental small intestinal bacterial overgrowth (SIBO) unrelated to jejunoileal bypass are susceptible to hepatic damage, possibly because of increased small intestinal permeability to proinflammatory bacterial polymers. However, data on the prevalence of hepatic damage in human subjects with SIBO in this setting are lacking. This study addressed this issue. METHODS: Seventy adult subjects were investigated for possible SIBO and hepatic damage with bacteriological analysis of small intestinal aspirates and measurement of serum concentrations of alkaline phosphatase, gamma-glutamyl transpeptidase, aspartate aminotransferase, and alanine aminotransferase. Nutritional indices (serum albumin and anthropometry) and the urinary lactulose/mannitol ratio, an index of small intestinal permeability, were measured in all subjects with SIBO and liver damage. RESULTS: SIBO was present in 40 of 70 subjects (57.1%). Overgrowth flora included salivary-type bacteria alone in 11 subjects and colonic-type bacteria in 29 subjects (facultative anaerobes [Enterobacteriaceae] alone in 21 subjects and both facultative and obligate anaerobes [Enterobacteriaceae and Bacteroides spp] in eight subjects). Biochemical evidence of liver damage was found in zero of 30 subjects without SIBO, zero of 11 subjects with SIBO with salivary-type bacteria alone, zero of 21 subjects with SIBO with facultative but not obligate anaerobic colonic-type bacteria, and in one of eight subjects (12.5%) with SIBO with obligate anaerobic colonic-type bacteria, in whom serum alkaline phosphatase and gamma-glutamyl transpeptidase levels were elevated. Nutritional indices were normal in this patient. Small intestinal permeability was increased and, along with liver enzyme abnormalities, normalized after eradication of SIBO. Small intestinal permeability was also increased in three of six patients (50.0%) with SIBO with obligate anaerobic colonic-type bacteria who had no evidence of liver damage. CONCLUSIONS: SIBO per se is not a major risk factor for liver damage in humans, even when the overgrowth flora includes obligate anaerobes. Liver damage is not a necessary consequence of increased small intestinal permeability in this setting.

Adolescent↗
PubMed2006

Low lactase activity in a small-bowel biopsy specimen: should dietary lactose intake be restricted in children with small intestinal mucosal damage?

OBJECTIVE: Small intestinal mucosal damage can result in decreased lactase activity (LA). When LA is low in a small-bowel biopsy (SBB) specimen, a reduction of dietary lactose intake is usually advised. This is often done by reducing dietary dairy products, which also reduces the intake of calcium, protein and vitamins. Since intestinal damage can have a patchy character and LA varies along the horizontal axis of the small intestine, the relevance of SBB measurement for intestinal LA could be questioned. We compared LA in the SBB with the in vivo capacity to digest lactose using the Lactose Digestion Index (LDI). MATERIAL AND METHODS: LA was measured in 18 children aged 0.8-10.9 years (mean 3.9, SD 2.4) undergoing SBB for various indications. In all children the LDI was determined using the (13)C-lactose/(2)H-glucose test. RESULTS: In 9/18 biopsy specimens LA was low (<10 U/g protein). LDI was normal in 14/18 patients. In 8 out of 9 patients with normal lactase activity, LDI was also normal, while in 6 out of 9 patients LDI was normal despite low LA in the biopsy. In patients with normal LDI, histology was normal in 6/14, in 4/14 mild histological changes (Marsh II) were seen and in 4 patients histological damage was severe (grade III). CONCLUSIONS: In children with small-bowel mucosal damage, lactose digestive capacity can remain high despite low LA and histological changes in an SBB. Extrapolation of LA in SBB specimens to overall lactose digestive capacity may not be reliable. The advice concerning the restriction of intake of dairy products cannot be based on the data of the SBB only.

Biopsy↗
PubMed1988

[Small intestine pouches as a therapeutic principle in stomach and large intestine replacement].

Small bowel pouches are being utilized in several versions as substitute reservoirs after total gastrectomy and after continence preserving proctocolectomy. Throughout the world, most frequently the pouch is formed by simple duplication of the gut. The principles of reservoir formation, the special functional requirement in the upper and lower GI-tract are delineated. Follow-up studies prove the successful use of gastric and ileoanal pouches.

Adenomatous Polyposis Coli↗
PubMed1986

Haemorrhage from idiopathic annular ulcers of the small intestine.

Annular small bowel ulceration is rare. We report three patients who presented with signs of chronic gastrointestinal blood loss. In two patients the main presenting symptom was intermittent abdominal pain while the third patient subsequently developed abdominal pain during the course of investigation. Preoperative localisation of the source of haemorrhage proved difficult in each case. However in all three patients an easily identifiable lesion was found at laparotomy. We believe that laparotomy should be undertaken more readily in the investigation of patients with the combination of abdominal pain and gastrointestinal bleeding as these patients are likely to have an anatomically identifiable cause for their symptoms.

Abdomen↗
PubMed1984

Localization of cholesterol synthesis in the small intestine of diabetic rats.

Previous studies have demonstrated that cholesterol synthesis is increased twofold in the small intestine of diabetic animals. The present study demonstrates that the stimulation of small intestinal cholesterol synthesis by diabetes is a generalized phenomenon occurring in all segments of the small intestine. Quantitatively, in control animals the proximal two segments of the small intestine account for the majority of the total small intestinal cholesterol synthesis, whereas in the diabetic animals, because of the generalized stimulation in cholesterogenesis, the contribution of the terminal segments to total small intestinal cholesterol synthesis is of increased importance. The various manipulations that regulate cholesterol synthesis in the small intestine of diabetic animals also affect cholesterol synthesis in all portions of the small intestine. In diabetic animals cholesterol feeding and the limitation of food intake decrease cholesterol synthesis in the total small intestine and in all segments of the small intestine. Conversely, colestipol feeding increases cholesterol synthesis in all segments of the small intestine. These results demonstrate that, despite the obvious structural, functional, and environmental differences among the various segments of the small intestine, the stimulation of cholesterol synthesis that occurs secondary to diabetes mellitus is a generalized phenomenon. Similarly, the factors that regulate small intestinal cholesterol synthesis do so in a generalized manner.

Animals↗
PubMed2006

Deficient UDP-glucuronosyltransferase detoxification enzyme activity in the small intestinal mucosa of patients with coeliac disease.

BACKGROUND: Small intestinal malignancies in humans are rare; however, patients with coeliac disease have a relatively high risk for such tumours. Intestinal UDP-glucuronosyltransferases are phase II drug metabolism enzymes also involved in the detoxification of ingested toxins and carcinogens. As many toxins and carcinogens are ingested via food, the human gastrointestinal tract not only has an important role in the uptake of essential nutrients, but also acts as a first barrier against such harmful constituents of the food. Therefore, the gastrointestinal mucosa contains high levels of detoxification enzymes such as cytochromes-P450, glutathione S-transferases and UDP-glucuronosyltransferases. AIM: To compare the UDP-glucuronosyltransferase detoxification capacity in small intestinal mucosa of patients with coeliac disease vs. that in normal controls. METHODS: We assessed UDP-glucuronosyltransferase enzyme activities towards 4-methylumbelliferone in small intestinal biopsies of patients with coeliac disease (n = 22) and age- and sex-matched controls (n = 27). RESULTS: Small intestinal UDP-glucuronosyltransferase enzyme activity in controls was significantly higher than in patients with coeliac disease: 0.55 +/- 0.27 vs. 0.35 +/- 0.16 nmol/min mg protein, respectively (mean +/- s.d., P = 0.005). DISCUSSION: The low small intestinal UDP-glucuronosyltransferase detoxification activity in patients with coeliac disease may result in a deficient detoxification of potential carcinogens, and thus could explain in part the relatively high small intestinal cancer risk in these patients.

Carcinogens↗
PubMed2004

Transporter mRNA expression in a conditionally immortalized rat small intestine epithelial cell line (TR-SIE).

Small intestine epithelial cell lines (TR-SIE), which are established from the small intestine of transgenic rats harboring temperature-sensitive simian virus 40 large T-antigen gene (tsA58 Tg rat), were used to characterize the mRNA expression of small intestine transporters. TR-SIE cells had a polygonal morphology and expressed cytokeratin protein and villin mRNA. Although the large T-antigen was strongly expressed at 33 degrees C, this was reduced at 37 and 39 degrees C. Concomitantly, the cell growth was arrested at 37 and 39 degrees C compared with that at 33 degrees C, suggesting that TR-SIE cells are conditionally immortalized cell lines. RT-PCR analysis revealed that TR-SIE cells expressed ABCB1 (mdr1a and mdr1b), ABCB4 (mdr2), ABCC2 (mrp2), ABCC6 (mrp6), ABCG1, ABCG2 (bcrp/mxr), Slc21a7 (Oatp3), Slc15a1 (PepT1), and Slc16a1 (Mct1). Conditionally immortalized rat small intestine epithelial cell lines were established from tsA58 Tg rats and expressed the mRNA of intestinal transporters.

Animals↗
PubMed1985

Mucosal lesions of the small intestine after intestinal vascular obstruction in the rat.

Small intestinal mucosal lesions, characteristically restricted to the villous tissue, have been described in shock states of different types. We have found this type of mucosal lesion in a standardized intestinal ischemia shock in rat. The pathophysiology of the mucosal lesion has been debated. In earlier work we noted a tenfold increase of platelets in the ischemic intestine. The importance of reperfusion and local platelet accumulation for the development of ischemic lesions in the intestinal mucosa was studied. Biopsy specimens taken immediately before and after reperfusion of the ischemic small intestine showed the same degree of mucosal lesion, i.e. total disintegration of the lamina propria. In thrombocytopenic rats subjected to intestinal ischemia, the severity of mucosal lesion was the same as in normothrombocytic rats. The results indirectly support the hypothesis of local villous oxygen deficit as the pathophysiologic mechanism leading to lesions of the small intestinal mucosa in shock.

Animals↗
PubMed1976

Primary malignant tumors of the small intestine.

Primary malignant tumors of the small intestine are uncommon. This infrequency and possible lack of awareness can result in a late diagnosis and a poor survival time. In a period of 34 years, only 55 patients were seen at our cancer institute. The average age of the patients was 56 years, with a male predominance ratio of 2.6:1.0. Twenty-one patients had adenocarcinomas, 19 had sarcomas and 15 had carcinoids. The most common signs and symptoms were abdominal pain and obstruction of the intestine. Preoperative diagnosis was established in 12 of these patients only by roentgenologic barium examination of the small intestine. At the time of diagnosis, 34 of the patients had metastasis to regional lymph nodes or distant organs. The median and five year survival times were one year and 19 per cent, respectively. Patients with carcinoids had better survival rates than those with adenocarcinomas or sarcomas. Palliative resection did not improve survival time. However, if other therapeutic modalities also were used, it might prove beneficial. Patients with palpable abdominal masses or intestinal bleeding, or both, had a worse prognosis than did those presenting with obstruction of the intestine because these are late presenting symptoms. Therefore, recurrent abdominal pain should increase clinical suspicion, and early diagnosis by careful examination of the small intestine with barium contrast material could improve the survival time. Finally, it seemed that these tumors had a high incidence of coexisting malignant conditions, as nine of the patients in our series had a second malignant tumor.

Adenocarcinoma↗
PubMed1986

Structural features of absorptive cell and microvillus membrane preparations from rat small intestine.

Absorptive cells of the small intestine are highly polarized cells with distinct microvillus membrane (MVM) and basolateral plasma membrane domains. We compared membrane structure in the following preparations of rat small intestine commonly used for in vitro study of MVM function: epithelial sheets, isolated epithelial cells, and four different MVM vesicle preparations, using electron microscopy of thin sections and freeze fracture replicas. We also quantitated mean vesicle diameter of the four MVM preparations by quasielastic light scattering and determined their actin content. Epithelial sheets maintained their plasma membrane polarity as judged by intramembrane particle (IMP) distribution for at least 30 min after isolation. In contrast, the plasma membrane of isolated cells showed redistribution of IMPs, indicating considerable loss of polarity in the few minutes required for cell recovery. The P-face IMPs in MVM prepared by Ca++ precipitation were randomly distributed but became aggregated after exposure to potassium thiocyanate, which removed approximately 50% of core actin. The P-face IMPs in Mg++ precipitated MVM were aggregated whether or not core actin was depleted with potassium thiocyanate. The shape and size of MVM vesicles differed considerably with different preparative techniques. The extremely rapid loss of plasma membrane polarity of isolated intestinal epithelial cells and the striking structural heterogeneity of MVM vesicles prepared by commonly used techniques should be considered in the interpretation of functional studies with these preparations.

Animals↗