Abstract

INTRODUCTION Some publications have demonstrated the presence of lung reperfusion injury in mesenteric ischemia and reperfusion (I/R), but under to diverse methods. Postconditioning has been recognized as effective in preventing reperfusion injury in various organs and tissues. However, its effectiveness has not been evaluated in the prevention of lung reperfusion injury after mesenteric ischemia and reperfusion.OBJECTIVE To evaluate the presence of pulmonary reperfusion injury and the protective effect of ischemic postconditioning on lung parenchyma in rats submitted to mesenteric ischemia and reperfusion.METHODS Thirty Wistar rats were distributed into three groups: group A (10 rats), which was held mesenteric ischemia (30 minutes) and reperfusion (60 minutes); group B (10 rats), ischemia and reperfusion, interspersed by postconditioning with two alternating cycles of reperfusion and reocclusion, for two minutes each; and group C (10 rats), ischemia and reperfusion interleaved by postconditioning with four alternating cycles of reperfusion and reocclusion of 30 seconds each. Finally, it was resected the upper lung lobe for histological analysis.RESULTS There were mild lung lesions (grade 1) in all samples. There was no statistical difference between groups 1 and 2 (P>0.05).CONCLUSION The mesenteric ischemia and reperfusion in rats for thirty and sixty minutes, respectively, caused mild reperfusion injury in lung. Postconditioning was not able to minimize the remote reperfusion injury and there was no difference comparing two cycles of two minutes with four cycles of 30 seconds.

Highlights

  • Some publications have demonstrated the presence of lung reperfusion injury in mesenteric ischemia and reperfusion (I/R), but under to diverse methods

  • Thirty Wistar rats were distributed into three groups: group A (10 rats), which was held mesenteric ischemia (30 minutes) and reperfusion (60 minutes); group B (10 rats), ischemia

  • Since 1986, when Parks & Granger[1] demonstrated the harmful effects of toxic reactive oxygen species (ROS) produced during reperfusion, many researches have been developed in search of an experimental model that could minimize this process in order to reduce the cellular and organic damage ischemia and reperfusion (I/R)[2,3]

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Summary

Introduction

Some publications have demonstrated the presence of lung reperfusion injury in mesenteric ischemia and reperfusion (I/R), but under to diverse methods. Its effectiveness has not been evaluated in the prevention of lung reperfusion injury after mesenteric ischemia and reperfusion. Since 1986, when Parks & Granger[1] demonstrated the harmful effects of toxic reactive oxygen species (ROS) produced during reperfusion, many researches have been developed in search of an experimental model that could minimize this process in order to reduce the cellular and organic damage ischemia and reperfusion (I/R)[2,3]. The best results ever published in controlling the production of ROS were obtained with the ischemic preconditioning, as numerous publications that followed Murry et al.[4], including the mesenteric I/R. In 2003, Zhao et al.[2] presented the concept of ischemic postconditioning (IPC), which consists of making one or more short cycles of reperfusion followed by one or more short cycles of ischemia, immediately after ischemia period and before to give permanent reperfusion.

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