02 March 2019 : Animal Research
[Retracted: 26 Aug 2019] Cardioprotective Effect of Isosorbide Dinitrate Postconditioning Against Rat Myocardial Ischemia-Reperfusion Injury In Vivo
Xinwen Zhao1ACDEF, Mengjuan Wang1BCDE, Mei Li2ABC, Na Wu3CFG, Dalin Song24ACDEFG*DOI: 10.12659/MSM.912814
Med Sci Monit 2019; 25:1629-1636
Abstract
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.
Keywords: Retracted Publication
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