On the specificity of altered muscle function in experimental colitis in rats

Grossi, Laurino; McHugh, Kevin J.; Collins, Stephen M.

doi:10.1016/0016-5085(93)90273-f

Cited by 95 publications

(53 citation statements)

References 23 publications

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“…In our model, evident morphological signs of inflammation disappeared in the second week after indomethacin treatment, whereas cyclical oscillation of motility, bacterial translocation, and inflammatory mediators continued to be present in the chronic phase. These findings agree with previous studies demonstrating that inflammation induces chronic changes at the structures controlling intestinal motor activity (6,16). Moreover, our studies demonstrate that structures controlling motor activity react to bacterial translocation and inflammation.…”

Section: Discussionsupporting

confidence: 93%

Intestinal motor disorders associated with cyclical bacterial overgrowth in a rat model of enteritis

Porras¹,

Martín²,

Soler³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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Porras, Monica, María Teresa Martín, Mercè Soler, and Patri Vergara. Intestinal motor disorders associated with cyclical bacterial overgrowth in a rat model of enteritis. Am J Physiol Gastrointest Liver Physiol 287: G58 -G64, 2004. First published February 12, 2004 10.1152/ajpgi.00513.2003.-The aims of this study were: 1) to obtain an experimental model reproducing the characteristics of chronicity and spontaneous relapses found in inflammatory bowel disease (IBD) and 2) to correlate these changes with intestinal motility and bacteria translocation. For this purpose, two groups of Sprague-Dawley rats were used: a treated group that received two subcutaneous injections of indomethacin (7.5 mg/kg) 48 h apart and a control group that received saline. Blood leukocytes, TNF, and fecal parameters were monitored for 90 days after treatment. In treated rats, a cyclic oscillation of blood leukocytes and TNF concomitant with an inverse correlation of fecal output was observed. Treated rats were then selected either during their highest or lowest blood leukocyte values for motor activity and microbiological evaluation. Controls were obtained in age-matched rats. Rats with high leukocyte levels showed a decrease of motor activity. In contrast, animals with low leukocyte levels presented hypermotility. Bacterial overgrowth accompanied by bacterial translocation was found in the group with high leukocytes, whereas no differences were observed between the control and indomethacin groups during the lowest leukocyte phase. We obtained a model of IBD characterized by a chronic cyclic oscillation of intestinal motility, flora, and inflammatory blood parameters. During the high-leukocyte stage, motor activity decrease is related to bacterial translocation. This phase is followed by a reactive one characterized by hypermotility associated with a decrease in both bacterial growth and leukocytes. However, as in IBD, this reaction seems unable to prevent a return to relapse. inflammatory bowel disease; gastrointestinal motility; gut flora; leukocytes INFLAMMATORY BOWEL DISEASE (IBD) in its more common forms, Crohn's disease (CD) and ulcerative colitis, is characterized by presenting alternative phases of activity and quiescence and by its chronicity (11). Several studies (12,22,29) indicate an abnormal immune reactivity to intestinal flora as the cause for the inflammation, probably caused by impairment of the mucosal barrier function.Systemic administration of indomethacin in the rat has been used to cause inflammation of the small intestine, which presents some histopathological similarities to lesions found in CD (5, 37). It has been suggested that inhibition of cyclooxygenase activity induced by this drug alters mucosal permeability (7), facilitating the entry of bacteria and other harmful substances into the lamina propia and producing inflammation (24). Luminal bacteria seems to be critical to the induction of intestinal damage, because both germ-free rats (24) and animals treated with antibiotics (8) develop minimal lesions a...

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Section: Discussionsupporting

confidence: 93%

Intestinal motor disorders associated with cyclical bacterial overgrowth in a rat model of enteritis

Porras¹,

Martín²,

Soler³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…2). This result is consistent with results of previous studies showing that circular smooth muscle contractility had decreased at 3-7 days after induction of colitis in human and rats (9,11,12). It has been demonstrated that inflammation of the intestine causes impairment of adrenergic, cholinergic, purinergic and nitrergic neurotransmission in the ENS (3,8,10,18).…”

Section: Discussionsupporting

confidence: 93%

Impairment and restoration of spontaneous contractile activity of longitudinal smooth muscles in the TNBS-inflamed hamster distal colon

et al. 2007

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In the present study, we aimed to determine how inflammation affects spontaneous motility in the longitudinal direction of a hamster colon preparation. Trinitrobenzene sulfonic acid (TNBS) injected into the distal colon caused diarrhea 4-7 days after the treatment, but diarrhea was not observed in hamsters kept for 4 weeks. At 1 week after induction of colitis, spontaneous motility in the longitudinal direction was strongly suppressed. Contraction of longitudinal smooth muscles induced by electrical field stimulation was impaired, but not that induced by exogenously applied acetylcholine, indicating that acute inflammation preferentially impairs neurotransmissions with a minor effect on contractility of the longitudinal smooth muscle itself. The spontaneous motility reappeared in the colonic preparation isolated from the hamster maintained for 4 weeks after induction of colitis. The reappearance of the motility accompanied cholinergic and nitrergic regulations of contractile activity. These results demonstrated that impairment and following restoration of spontaneous contractile activity of longitudinal smooth muscles in the TNBS-inflamed distal colon of the hamster may depend on the damage and recovery of neural factors, rather than alteration of muscle contractility.

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“…In addition, activation or no change in sodium pump activity together with suppression of NHE-1 (in the present study) may result in the diminution of intracellular Na + , which might decrease the intracellular Ca 2+ level. Thus, a reduced Ca 2+ level may be a factor responsible for decreased contractility reported earlier in these conditions (36,37). Nevertheless, these changes do not seem to be due to a parallel increase in the crude microsomes or total RNA yield in both cases.…”

Section: Discussionmentioning

confidence: 63%

Role of Na⁺/H⁺Exchanger Isoform-1 in Human Inflammatory Bowel Disease

Khan

Siddique

Al-Awadi

et al. 2003

Canadian Journal of Gastroenterology

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BACKGROUND: Na + /H + exchanger (NHE) is responsible for a net uptake of sodium chloride and water from the gastrointestinal tract and maintains electrolyte and water homeostasis. However, its status in human inflammatory bowel disease such as ulcerative colitis (UC) and Crohn's disease (CD) remains poorly understood. OBJECTIVES: To investigate the role of NHE-1 isoform in human CD and UC. METHODS: Expression of NHE-1 protein and messenger ribonucleic acid and sodium pump activity were examined in the colonic biopsy samples taken from UC (n=11) and CD (n=13) patients using enhanced chemiluminescence-Western blot analysis, reverse transcription polymerase chain reaction and spectrophotometry. Subjects presenting with abdominal pain and endoscopically normal colon served as normal controls (n=11). Myeloperoxidase (MPO) activity and histology were performed to confirm tissue inflammation. RESULTS: MPO activity increased significantly (P<0.05) in both UC and CD patients compared with the normal controls. Parallel to MPO activity profile, there was also a significantly higher infiltration of inflammatory cells in both cases. P-nitrophenylphosphatase activity, a marker of the sodium pump, remained unchanged in CD but increased significantly (P<0.05) in UC compared with the normal controls. On the contrary, the level of NHE-1 protein and messenger ribonucleic acid was significantly decreased (P<0.05) in both cases, whereas the internal control, a-actin remained unaltered. CONCLUSIONS: These findings demonstrate a transcriptionally regulated suppression of NHE-1 in both UC and CD. This NHE-1 suppression may reduce an uptake of sodium chloride and water from the inflamed colonic lumen and thus contribute to diarrhea and neuromuscular alterations in these conditions.

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On the specificity of altered muscle function in experimental colitis in rats

Cited by 95 publications

References 23 publications

Intestinal motor disorders associated with cyclical bacterial overgrowth in a rat model of enteritis

Intestinal motor disorders associated with cyclical bacterial overgrowth in a rat model of enteritis

Impairment and restoration of spontaneous contractile activity of longitudinal smooth muscles in the TNBS-inflamed hamster distal colon

Role of Na⁺/H⁺Exchanger Isoform-1 in Human Inflammatory Bowel Disease

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On the specificity of altered muscle function in experimental colitis in rats

Cited by 95 publications

References 23 publications

Intestinal motor disorders associated with cyclical bacterial overgrowth in a rat model of enteritis

Intestinal motor disorders associated with cyclical bacterial overgrowth in a rat model of enteritis

Impairment and restoration of spontaneous contractile activity of longitudinal smooth muscles in the TNBS-inflamed hamster distal colon

Role of Na+/H+Exchanger Isoform-1 in Human Inflammatory Bowel Disease

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Role of Na⁺/H⁺Exchanger Isoform-1 in Human Inflammatory Bowel Disease