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

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/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.

Postconditioning with Nitrates Protects Against Myocardial Reperfusion Injury: A New Use for an Old Pharmacological Agent

“…Finally, they can prevent adverse remodeling in patients who fail in reperfusion. Zhao et al investigated the cardioprotective effect of isosorbide dinitrate (ISDN) postconditioning against rat RI in vivo, and demonstrated that ISDN postconditioning induces a similar cardioprotective effect as I-PostC via improvement of myocardial antioxidant capacity [82]. Nitrate redistributes coronary flow to the ischemic regions of the heart, which was initially observed by measuring the oxygen saturation in large and small arteries of the coronary circulation in vivo [83].…”

Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation

“…Because of its timing, IPC could be used in clinical reperfusion settings involving direct angioplasty, and it has been shown to reduce infarct size and prevent reperfusion-induced endothelial dysfunction in humans 2,3 . Nowadays, IPC has been demonstrated to alleviate myocardial I/R injury in various models 8,9 . Several mechanisms have been implicated in this novel strategy, including the suppression of inflammation 10 .…”

Cytoprotective Effects of Dinitrosyl Iron Complexes on Viability of Human Fibroblasts and Cardiomyocytes

“…The most common drugs in term of treatment cardiovascular disease are nitroglycerin, nitrosorbid, nitroprusside, and nitrite, which release NO in cells and tissues during their metabolism (Münzel and Schulz, 2010; Kapelko et al, 2017; Gatzke et al, 2018; Liu et al, 2019; Lu et al, 2019; Zhao et al, 2019). However, these drugs are often unstable, non-specific, toxic, and have a number of side effects (Tardiolo et al, 2019).…”