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Cardioprotective effects of cyclosporine A in an in vivo model of myocardial ischemia and reperfusion
Author(s) -
Xie J.R.,
Yu L.N.
Publication year - 2007
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.2007.01342.x
Subject(s) - medicine , in vivo , myocardial ischemia , ischemia , myocardial reperfusion injury , cardiology , reperfusion injury , pharmacology , microbiology and biotechnology , biology
Background: Recent evidence indicates that reperfusion of the heart after a period of ischemia leads to the opening of the mitochondrial permeability transition pore (MPTP). The aim of this study was to investigate cardioprotective effects of cyclosporine A (CsA), an inhibitor of the MPTP, in an in vivo model of myocardial ischemia and reperfusion. Methods: Male Sprague–Dawley rats were subjected to occlusion of the left anterior descending coronary artery for 30 min followed by 180 min of reperfusion. CsA (10 mg/kg) or vehicle was given 10 min prior to ischemia via the femoral vein. Sham myocardial ischemia–reperfusion rats (sham‐operation group) were used as controls. Infarct size was measured using the staining agent TTC (2,3,5‐triphenyl tetrazolium chloride) and myocardial apoptosis by caspase‐3 activity was determined by fluorescent assay. The myocardium mitochondria ultrastructure was observed through a transmission electron microscope. Results: CsA significantly reduced infarct size (48.8 ± 5.8% of left ventricle in vehicle + I/R group and 30.3 ± 2.7% of left ventricle in CsA + I/R, respectively) and decreased caspase‐3 activity in the myocardium [(0.62 ± 0.17)/μg of protein and (0.42 ± 0.15)/μg of protein, respectively] and relieved the injury of mitochondria. Conclusion: CsA reduced the cardiac damage associated with ischemia–reperfusion injury of the heart. The cardioprotective effects of CsA might be associated with the protection of mitochondria and the inhibition of caspase‐3 activity. It also suggests that the MPTP might play an important role in cardiomyocytes death after ischemia–reperfusion injury.