The effect of levosimendan on myocardial ischemia reperfusion injury in rats

Depending on the duration of ischemia, reactive oxygen species (ROS), which are related to cellular injury, may occur after I/R injury of various etiology. As a consequence, structural deterioration is caused by free oxygen radicals increasing within the cell. Cytokines, which activate a series of reactions that cause tissue damage and inflammatory response, are released during reperfusion of ischemic tissues. In this study, we aimed to compare the effects of levosimendan on ischemia/reperfusion injury. Twenty-four rats are randomly divided into four groups: Group C (n = 6):control; Group I/R (n=6): ischemia/reperfusion; Group I/R-LAI (n=6): ischemia/reperfusion-levosimendan after ischemia; and Group I/R-LBI (n=6):ischemia/reperfusion-levosimendan before ischemia. Heart tissue samples were obtained following 45 minutes of ischemia and 90 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 lower in Group I/R-LBI than in Group I/R.SOD levels were significantly lower in Group I/R than in the Group C. Further, SOD levels were significantly higher in Group I/R-LBI than in Group I/R. GST and CAT levels were similar in all groups. Myonecrosis in Group IR was significantly higher than in Group C. Additionally, myonecrosis in groups IR-LBI and IR-LAI 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. In addition, edema was found to be significantly lower in groups IR-LAI and I/R-LBI than in Group IR. Based on the results, we believe that, the protective effects of levosimendan on ischemia-reperfusion injury will be shown in detail and indication for use will be expanded, with support from other studies .