The effect of dexametidin on ischemia reperfusion injury in myocart of rat

The Effect of Dexmedetomidin on Myocardial Ischemia Reperfusion Injury in Rats Depending on the duration of ischemia, reactive oxygen species (ROS), which are related to cellular injury, may ocur after I/R injury of various etiology. As a consequence, structural deterioration is caused by free oxygen radicals increasing within the cell. Cytokines, which activatea series of reactions that cause tissue damage and inflammatory response, are released during reperfusion of ischemic tissues. In this study, weaimed to compare the effects of dexmedetomidin ischemia/reperfusion injury. Twenty-four rats are randomly divided in to four groups: Group C(n = 6): control; Group IR(n=6): ischemia/reperfusion; Group IR-D (n=6): ischemia/reperfusion-dexmedetomidin after ischemia; and Group D (n=6):dexmedetomidin Heart tissue samples were obtained following 60 minutes of ischemia and 120 minutes of the reperfusion period to assess MDA, SOD, GSH and CAT levels. Histopatholojical parameters were also compared. MDA levels were significantly higher in Group IR than in the Group C. Further, MAD Levels were significantly lowerin Group IR-D than in Group IR. SOD levels were significantly lower in Group IR than in the Group C. Further, SOD Levels were significantly higherin Group IR-D than in Group I/R. GST and CAT levels were similarin all groups. Myonecrosis in Group IR was significantly higher than in Group C. Additionally, myonecrosis in groups IR-D was found to be significantly lower than in Group IR. Cell infiltration in Group IR were significantly higher than Group C. Edema was found to be significantly higher in Group IR than in Group C. Inaddition, edema was found to be significantly lower in groups IR-D than in Group IR. Based on the results, we believe that, the protective effects of dexmedetomidin on ischemia-reperfusion injury will be shown in detail and indication for use will be expanded, with support from other studies .