Abstract

To investigate the action of pentoxifylline (PTX) and prostaglandin E1 (PGE1) on ischemia and reperfusion of small intestine tissue in rats, using immunohistochemical analysis. Thirty-five Wistar rats were distributed as follows: group A (n=10): subjected to intestinal ischemia and reperfusion for 60 min, with no drugs; group B (n=10): PTX given during tissue ischemia and reperfusion; group C (n=10): PGE1 given during tissue ischemia and reperfusion; group D (n=5): sham. A segment of the small intestine was excised from each euthanized animal and subjected to immunohistochemical examination. Mean number of cells expressing anti-FAS ligand in the crypts was highest in Group A (78.9 ± 17.3), followed by groups B (16.7 ± 2.8), C (11.3 ± 1.8), and D (2.5 ± 0.9), with very significant differences between groups (p<0.0001). The use of pentoxifylline or prostaglandin E1 proved beneficial during tissue reperfusion. The immunohistochemical results demonstrated a decrease in apoptotic cells, while protecting other intestinal epithelium cells against death after reperfusion, allowing these cells to renew the epithelial tissue.

Highlights

  • Sudden interruption of arterial blood flow causes tissue ischemia, which triggers an array of metabolic changes in the ischemic territory, making tissue repair dependent on early restoration of blood flow[1]

  • The extent of damage caused by ischemia depends on location of the arterial occlusion, availability of collateral circulation, oxygen demand by the tissues involved, and time elapsed between ischemia and reperfusion[2,3]

  • prostaglandin E1 (PGE1) has strong vasodilating action and plays a role in activating fibrinolysis and modulating cell proliferation, as well as in fibrogenesis, angiogenesis, and tissue fibrinolysis[11,12]. Considering these aspects, the purpose of the present study was to perform an immunohistochemical evaluation of PTX and PGE1 ability to attenuate lesions in the small intestine of rats subjected to ischemia and reperfusion

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Summary

Introduction

Sudden interruption of arterial blood flow causes tissue ischemia, which triggers an array of metabolic changes in the ischemic territory, making tissue repair dependent on early restoration of blood flow[1]. A systematic review of the literature[4] demonstrated the importance of elucidating biochemical processes for a better comprehension of the reactions triggered after ischemia and reperfusion This body of published data has led to the use of drugs capable of minimizing the deleterious effects of ischemia-reperfusion on small intestine tissues[4]. Owing to their antioxidative ability, pentoxifylline (PTX) and prostaglandin E1 (PGE1) directly inhibit superoxide anions, which indirectly block the action of xanthine oxidase. PGE1 has strong vasodilating action and plays a role in activating fibrinolysis and modulating cell proliferation, as well as in fibrogenesis, angiogenesis, and tissue fibrinolysis[11,12]

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