08 March 2019 : Animal Research
The Cardioprotective Effects of Remote Ischemic Conditioning in a Rat Model of Acute Myocardial Infarction
Li You12BCE, Ying-Ying Pan13CDF, Meng-Yao An1DEF, Wen-Hua Chen4BD, Ying Zhang1BC, Yan-Na Wu1CDF, Yan Li1BE, Kai Sun1CDE, Yong-Qiang Yin1BE, Jian-Shi Lou1AG*DOI: 10.12659/MSM.914916
Med Sci Monit 2019; 25:1769-1779
Abstract
BACKGROUND: Cardiac remote ischemic conditioning (RIC) is a noninvasive cardioprotective method in ischemia-reperfusion injury and acute myocardial infarction (AMI). The aims of this study were to investigate the effects of RIC in a rat model of AMI.
MATERIAL AND METHODS: Adult male Sprague-Dawley rats included the AMI group that underwent ligation of the left anterior descending (LAD) coronary artery (n=24), the RIC group that consisted the AMI rat model treated with RIC once daily in the left hind limb until days 1, 7 and 14 (n=24), and the sham group (n=24). Myocardial infarct size was measured by routine histology with triphenyltetrazolium chloride (TTC) and Masson’s trichrome histochemical staining for myocardial necrosis and fibrosis, respectively. Serum levels of Bcl-2, Bax, caspase-3, and inducible nitric oxide synthase (iNOS) were measured by enzyme-linked immunosorbent assay (ELISA). The apoptosis index was detected using the TUNEL assay. Spectrophotometry of the myocardium was used to identify mitochondrial complexes and myocardial ATP.
RESULTS: The RIC group showed improved cardiac hemodynamics, reduced the size of the myocardial infarction, upregulated expression of Bcl-2, and down-regulation of the levels of Bax, caspase-3, and iNOS, and reduced cardiac myocyte apoptosis and inhibited the opening of the mitochondrial permeability transition pore (MPTP).
CONCLUSIONS: In a rat model of AMI, RIC improved the hemodynamic index, reduce the levels of apoptosis and myocardial injury, and improved mitochondrial function.
Keywords: Endomyocardial Fibrosis, Mitochondria, Cardiotonic Agents, Heart Injuries, Hemodynamics, Ischemic Preconditioning, Myocardial Reperfusion Injury, Myocardium, Proto-Oncogene Proteins c-bcl-2, bcl-2-Associated X Protein
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