28.02.2014 Aufrufe

Effekt selektiver und nicht selektiver nichtsteroidaler Antiphlogistika ...

Effekt selektiver und nicht selektiver nichtsteroidaler Antiphlogistika ...

Effekt selektiver und nicht selektiver nichtsteroidaler Antiphlogistika ...

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Summary<br />

In the analysis an infiltration of neutrophils was fo<strong>und</strong> in the muscularis externa and<br />

serosa of the injured jejunum samples after ischemia and reperfusion. Even the nonmanipulated<br />

control samples showed a significant infiltration with neutrophils. This<br />

indicates a inflammatory response of the whole bowl which needs to be investigated<br />

in a future study. The esinophils were fo<strong>und</strong> only rarely and isolated in the muscularis<br />

externa and serosa. That indicates an inferior role of eosinophils for the inflammation<br />

reaction caused by ischemia and reperfusion. The COX-1 was expressed constitutive<br />

in several strong characteristics in the circulare muscle of the muscularis externa of<br />

the equine jejunum. COX-2 presented itself as an inducible enzyme through ischemia<br />

and reperfusion. The expression in the muscularis was less than COX-1 and was<br />

fo<strong>und</strong> particularly in the longitudinal muscle of the muscularis externa. Moreover, the<br />

endothelial cells and very likely fibrocytes, as well as lymphocytes and macrophages<br />

were similar to COX-1 and COX-2 positive. There was no significant difference<br />

between the different flunixin meglumin <strong>und</strong> firocoxib samples regarding neither<br />

neutrophils and eosinophils nor COX-1 and COX-2 producing cells.<br />

The study showed that ischemia and reperfusion induce neutrophile inflammation in<br />

the muscularis externa of the jejunum, even in non-manipulated control samples on<br />

which the NSAIDs did not have an influence. Moreover, the study revealed a different<br />

expression of COX-1 and COX-2 in the circulare and longitudinal muscle of the<br />

muscularis externa, which was constitutive for the COX-1 and inducible for the<br />

COX-2.<br />

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