Cardioprotective Effect of Isosorbide Dinitrate Postconditioning Against Rat Myocardial Ischemia-Reperfusion Injury In Vivo.

BACKGROUND This study investigated the cardioprotective effect of isosorbide dinitrate (ISDN) postconditioning against rat myocardial ischemia/reperfusion injury in vivo and provided a theoretical basis for clinical application. MATERIAL AND METHODS We randomly divided 32 Wistar rats into 4 groups: sham group, I/R (ischemia/reperfusion) group, I-PostC group (with 3 cycles of 30 s reperfusion and 30 s reocclusion applied at the onset of reperfusion), and P-PostC group (nitrate postconditioning: isosorbide dinitrate (5mg/kg) was given 1 min before reperfusion). The left anterior descending artery (LAD) was occluded for 40 min, followed by a 180-min reperfusion. Relevant indicators were tested. The LAD was occluded again, then we determined the myocardial infarct size. Paraffinized sections were prepared and TUNEL detection was performed. RESULTS There were no significant differences in ischemic sizes between different groups. Compared with the I/R group, the levels of cTnI and myocardial infarct size in the I-PostC group and P-PostC group were significantly decreased (p<0.05). However, there were no significant difference between the I-PostC group and P-PostC group. Compared with the sham-operated group, the levels of cTnI and MDA in the I/R group, I-PostC group, and P-PostC group were significantly increased (p<0.05) and the levels of SOD were significantly decreased (p<0.05). Compared with the I/R group, I-PostC and P-PostC decreased the level of MDA and increased the level of SOD (both P<0.05). CONCLUSIONS ISDN postconditioning induces a similar cardioprotective effect as I-PostC. The potential mechanisms of cardioprotection of ISDN postconditioning might be via improvement of myocardial antioxidant capacity and reduced generation of reactive oxygen species.