Indomethacin-Induced Disturbances in Villous Microcirculation in the Rat Ileum

Ruh, Joachim; Schmidt, E.; Vogel, Frank; Klar, E.

doi:10.1006/mvre.1999.2162

Cited by 16 publications

(14 citation statements)

References 15 publications

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“…Normal values were measured after 15 days. In indomethacin-induced jejunal inflammation, intravital microscopy has documented an increase in villous perfusion at 24 h accompanied by a significant decrease 7 days after systemic administration of indomethacin [22]. A decrease in colonic blood flow was also demonstrated in rats with acute colitis induced by acetic acid [6].…”

Section: Discussionmentioning

confidence: 84%

Blood flow alterations in TNBS-induced colitis: Role of endothelin receptors

2004

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Section: Discussionmentioning

confidence: 84%

Blood flow alterations in TNBS-induced colitis: Role of endothelin receptors

2004

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“…However, because the described protocols using indomethacin cause extensive intestinal damage (19,37), studies could only be performed a few (27), we obtained rats with less-severe lesions, which allowed us to perform chronic studies. As previously reported (37), an initial inflammatory reaction was observed especially in the mid-small intestine, which was concomitant with enterobacteria overgrowth and wall invasion by both enterobacteria and gram-positive bacteria.…”

Section: Discussionmentioning

confidence: 99%

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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“…In indomethacin-induced jejunal inflammation, intravital microscopy has documented capillary vasoconstriction and microthrombi formation before progressing to the mucosal inflammation and ulceration characteristic of Crohn's disease [16,17]. Finally, trinitrobenzene sulphonic acid induced colitis which results in a severe transmural and granulomatous inflammation has similarly been shown by micro-angiopathy to be preceded by small vessel thrombotic occlusion [18].…”

Section: Microvascular Anatomymentioning

confidence: 96%

Crohn's disease: in defense of a microvascular aetiology

Thornton

Solomon

2002

Int J Colorectal Dis

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Proving cause and effect will always be a difficult task given the self-perpetuating nature of the inflammatory and coagulation cascades and our inability at present to identify persons who subsequently develop Crohn's disease at a point prior to mucosal inflammation. Results to date however, are supportive of each of these factors, alone or in combination playing an integral part in the development of microvascular ischaemia, a pathological process which appears to precede the classic changes which characterize Crohn's disease.

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Indomethacin-Induced Disturbances in Villous Microcirculation in the Rat Ileum

Cited by 16 publications

References 15 publications

Blood flow alterations in TNBS-induced colitis: Role of endothelin receptors

Blood flow alterations in TNBS-induced colitis: Role of endothelin receptors

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

Crohn's disease: in defense of a microvascular aetiology

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