Selective COX-2 Inhibition Reduces Leukocyte Sticking and Improves the Microcirculation in TNBS Colitis

Kruschewski, M.; Anderson, Tanja; Buhr, H. J.; Loddenkemper, Christoph

doi:10.1007/s10620-006-3189-9

Cited by 10 publications

(7 citation statements)

References 68 publications

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“…In contrast to our T-cell transfer model, enhanced hypoxia with TNBS is not likely related to hematocrit, with the TNBS-induced increase in hematocrit speculated to be due to a fluid shift out of the circulation due to increased vascular permeability (12). …”

Section: Discussioncontrasting

confidence: 84%

Relationship between inflammation and tissue hypoxia in a mouse model of chronic colitis

Carter¹,

Yadav²,

Watts³

et al. 2011

Inflammatory Bowel Diseases

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Background-Hypoxia has been reported to be associated with the colonic inflammation observed in a chemically induced mouse model of self-limiting colitis suggesting that low tissue oxygen tension may play a role in the pathophysiology of inflammatory tissue injury. However, no studies have been reported evaluating whether tissue hypoxia is associated with chronic gut inflammation. Therefore, the objective of the present study was to determine whether hypoxia is produced within the colon during the development of chronic gut inflammation.

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Section: Discussioncontrasting

confidence: 84%

Relationship between inflammation and tissue hypoxia in a mouse model of chronic colitis

Carter¹,

Yadav²,

Watts³

et al. 2011

Inflammatory Bowel Diseases

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“…Buhr and colleagues (7,(21)(22)(23), using intravital microscopy, have repeatedly observed an increased mucosal blood flow within 24 h after induction of colitis with TNBS and a reduced blood flow after 3 days. Deniz et al (6) recorded decreased arterial mesenteric blood flow at early stages in TNBS-induced colitis in mice.…”

Section: Discussionmentioning

confidence: 99%

“…The regulation of colonic mucosal blood flow is poorly understood, and its importance during colonic injury is still unclear. Studies in recent years have yielded contradictory data, showing either an increased (8,11,14,27) or a decreased (7,11,21,22,38) blood flow in different animal models of colitis, using a variety of measuring techniques. The few blood flow studies conducted in humans with IBD have indicated that the mucosal blood flow is increased in inflamed regions (3,15).…”

mentioning

confidence: 99%

eNOS involved in colitis-induced mucosal blood flow increase

Petersson¹,

Schreiber²,

Steege³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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The role of NO in inflammatory bowel disease is controversial. Studies indicate that endothelial nitric oxide synthase (eNOS) might be involved in protecting the mucosa against colonic inflammation. The aim of this study was to investigate the involvement of nitric oxide (NO) in regulating colonic mucosal blood flow in two different colitis models in rats. In anesthetized control and colitic rats, the distal colon was exteriorized and the mucosa visualized. Blood flow (laser-Doppler flowmetry) and arterial blood pressure were continuously monitored throughout the experiments, and vascular resistance was calculated. Trinitrobenzene sulfonic acid (TNBS) or dextran sulfate sodium (DSS) was used to induce colitis. All groups were given the NOS inhibitor N(omega)-nitro-l-arginine (l-NNA) or the inducible NOS (iNOS) inhibitor l-N(6)-(1-iminoethyl)-lysine (l-NIL). iNOS, eNOS, and neuronal NOS (nNOS) mRNA in colonic samples were investigated with real-time RT-PCR. Before NOS inhibition, colonic mucosal blood flow, expressed as perfusion units, was higher in both colitis models compared with the controls. The blood flow was reduced in the TNBS- and DSS-treated rats during l-NNA administration but was not altered in the control group. Vascular resistance increased more in the TNBS- and DSS-treated rats than in the control rats, indicating a higher level of vasodilating NO in the colitis models. l-NIL did not alter blood pressure or blood flow in any of the groups. iNOS and eNOS mRNA increased in both colitis models, whereas nNOS remained at the control level. TNBS- and DSS-induced colitis results in increased colonic mucosal blood flow, most probably due to increased eNOS activity.

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“…They demonstrated that these drugs exert a significant attenuation of the extent and severity of the histological signs of cell damage, significant reduction in tissue PGE 2 production, as well reduction in NOS activity. The acute phase of TNBS colitis is characterized by a significant reduction of capillary blood flow, capillary density, diuresis, and weight and a significant increase in capillary permeability, leukocyte sticking, and hematocrit (Kruschewski et al, 2006). Kruschewski et al (2006) demonstrated that the selective COX-2 inhibitor NS-398 leads to a significant improvement of all microcirculatory parameters and clinical findings compared to the (untreated) colitis.…”

Section: Studymentioning

confidence: 99%

“…The acute phase of TNBS colitis is characterized by a significant reduction of capillary blood flow, capillary density, diuresis, and weight and a significant increase in capillary permeability, leukocyte sticking, and hematocrit (Kruschewski et al, 2006). Kruschewski et al (2006) demonstrated that the selective COX-2 inhibitor NS-398 leads to a significant improvement of all microcirculatory parameters and clinical findings compared to the (untreated) colitis. On the other hand, Reuter et al (1996) reported that administration of three types of COX-2 inhibitors with moderate to high selectivity significantly exacerbated the severity of colonic damage in experimental colitis.…”

Section: Studymentioning

confidence: 99%