to be primarily mediated by the release of PAF postischaemic gut. It was observed that sPLA2 inhibitor some protection against intestinal I Rinduced hypotension, in agreement with the hypothesis that PAF plays a r showed Important in mediating this response. In contrast, COX celebrex and flunixin not prevent intestinal IR-induced IC-87114 hypotension. Interestingly, leukotriene receptor antagonist zafirlukast was also some protection, suggesting some involvement of leukotrienes in the intestinal IR-induced hypotension. Histopathological examination clearly showed the effects of protective fabric of various drugs in the pretreatment of the intestine I. R. The mucosa is the metabolically active layer in the intestinal wall and, therefore, is the first layer of the fabric to show signs of Ish Chemistry.
The first process changes Darmisch in Chemistry were observed, are at the top of the villi. Less than 10 minutes ish Mie be ultrastructural Ver Detectable changes and Zellsch Ending is extensive in 30 minutes. Pull the ends of the villi of the small intestine and the surface chenschicht Through the lining of the intestine The H Morrhagie necrosis and transmural submucosal sq.m follows possible. In this study, the animals showed a farce, little or no histological Ver Changes in the small intestine, but significant Sch Caused the IR villi of the small intestine. The iv administration of either pre-or sPLA2 inhibitor zafirlukast strongly protected in the intestine.
Conversely, pretreatment with iv celebrex or flunixin intravenously S changes provided less protection against intestinal IR-induced histopathological Ver, Suggesting that prostaglandins k Can play an r Protector in the intestinal mucosa after Pajdo R. et al using a rat model of isch Mix Pr conditioning Determine the r prostaglandins found there gastric isch mix Pr conditioning a protective effect against IR injury time, the prostaglandins from COX-1 and COX-2-derived enzymes implies stimulated. Moreover, it was found that endogenous prostaglandin of COX enzymes derived in the mechanism of recovery of mucosal erosion induced acute gastric IR P involved the oral administration of the inhibitor of sPLA2 have provided less protection against histopathological changes Ver That intravenously Se administration, suggesting that our method of oral or oral bioavailability intrinsic inhibitor did not provided enough blood than intravenously s protection against intestinal L emissions.
On the other hand we have shown that the intravenous Se administration in a blood concentration of the inhibitor, which was much h Ago than after oral administration of the same dose. Better protection against injury of intestinal tissue with h Heren oral doses were found. Obviously there are many mediators of inflammation and Sch Ending mechanisms in diseases causing intestinal IR tha