Korean Circulation Journal

The Korean Society of Cardiology (대한심장학회)
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AT1 Receptor Modulator Attenuates the Hypercholesterolemia-Induced Impairment of the Myocardial Ischemic Post-Conditioning Benefits

  • Li, Yun-Wei (Department of Cardiology, Henan University Huaihe Hospital) ;
  • Li, Yan-Ming (Department of Cardiology, Henan University Huaihe Hospital) ;
  • Hon, Yan (Department of Cardiology, Henan University Huaihe Hospital) ;
  • Wan, Qi-Lin (Department of Cardiology, Henan University Huaihe Hospital) ;
  • He, Rui-Li (Department of Cardiology, Henan University Huaihe Hospital) ;
  • Wang, Zhi-Zhong (Department of Cardiology, Henan University Huaihe Hospital) ;
  • Zhao, Cui-Hua (Department of Cardiology, Henan University Huaihe Hospital)
  • Received : 2015.10.14
  • Accepted : 2016.04.14
  • Published : 2017.03.31
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Abstract

Background and Objectives: Ischemic post-conditioning (PostC) has been demonstrated as a novel strategy to harness nature's protection against myocardial ischemia-reperfusion (I/R). Hypercholesterolemia (HC) has been reported to block the effect of PostC on the heart. Angiotensin II type-1 (AT1) modulators have shown benefits in myocardial ischemia. The present study investigates the effect of a novel inhibitor of AT1, azilsartan in PostC of the heart of normocholesterolemic (NC) and HC rats. Materials and Methods: HC was induced by the administration of high-fat diet to the animals for eight weeks. Isolated Langendorff's perfused NC and HC rat hearts were exposed to global ischemia for 30 min and reperfusion for 120 min. I/R-injury had been assessed by cardiac hemodynamic parameters, myocardial infarct size, release of tumor necrosis factor-alpha troponin I, lactate dehydrogenase, creatine kinase, nitrite in coronary effluent, thiobarbituric acid reactive species, a reduced form of glutathione, superoxide anion, and left ventricle collagen content in normal and HC rat hearts. Results: Azilsartan post-treatment and six episodes of PostC (10 sec each) afforded cardioprotection against I/R-injury in normal rat hearts. PostC protection against I/R-injury was abolished in HC rat hearts. Azilsartan prevented the HC-mediated impairment of the beneficial effects of PostC in I/R-induced myocardial injury, which was inhibited by L-$N^5$-(1-Iminoethyl)ornithinehydrochloride, a potent inhibitor of endothelial nitric oxide synthase (eNOS). Conclusion: Azilsartan treatment has attenuated the HC-induced impairment of beneficial effects of PostC in I/R-injury of rat hearts, by specifically modulating eNOS. Azilsartan may be explored further in I/R-myocardial injury, both in NC and HC conditions, with or without PostC.

Keywords

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