AT1 Receptor Modulator Attenuates the Hypercholesterolemia-Induced Impairment of the Myocardial Ischemic Post-Conditioning Benefits

Figures

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  Fig. 1. Diagrammatic representation of experimental protocol. NC: normocholesteroleic, I/R: ischemia-reperfusion, I: ischemia, R: reperfusion, L-NIO: L-N5-(1-Iminobutyl)ornithine hydrochloride, HCI: hydrochloric acid, HC: hypercholeterolemic, S: stablization, P: perfusion, K-H: Krebs Henseleit.

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  Fig. 2. Effect of azilsartan perfusion on the hemodynamic parameters of an isolated heart in ischemia-reperfusion injury and ischemic-post conditioning of normal and hypercholesterolemic rats. Results are expressed as mean±standard deviation. ap<0.05 vs. sham control group; bp<0.05 vs. I/R-NC group; cp<0.05 vs. sham control-HC group; dp<0.05 vs. I/R-HC group; ep<0.05 vs. AZ+PostC-I/R-HC group. BMP: beats per minute, NC: normocholesterolemic, I/R: ischemia-reperfusion, PostC: post-conditioning, AZ: azilsartan, HC: hypercholesterolemic, L-NIO: selective eNOS inhibitor, LVEDP: left ventricular end-diastolic pressure, LVPP: left ventricular protection period.

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  Fig. 3. Effect of azilsartan perfusion on (A) LDH, (B) K-MB and (C) TNF-α in ischemia-reperfusion injury and ischemic-post conditioning of normal and hypercholesterolemic rats. Results are expressed as mean±standard deviation. ap<0.05 vs. sham control-NC group. bp<0.05 vs. I/R-NC group. cp<0.05 vs. sham control-HC group. dp<0.05 vs. I/R-HC group. ep<0.05 vs. AZ+PostC-I/R-HC group. LDH: lactate dehydrogenase, CK-MB: creatine kinase, TNF-α: tumor necrosis factor-alpha, NC: normocholesterolemic, I/R: ischemia-reperfusion, NC: normocholesterolemic, PostC: post-conditioning, HC: hypercholesterolemic, AZ: azilsartan, L-NIO: selective eNOS inhibitor.

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  Fig. 4. Effect of azilsartan perfusion on (A) nitrite levels and (B) TnI in ischemia-reperfusion injury and ischemic-post conditioning of normal and hypercholesterolemic rats. Results are expressed as mean±standard deviation. ap<0.05 vs. sham control-NC group. bp<0.05 vs. I/R-NC group. cp<0.05 vs. sham control–HC group. dp<0.05 vs. I/R-HC group. ep<0.05 vs. AZ+PostC-I/R–HC group. TnI: troponin-I, NC: normocholesterolemic, HC: hypercholesterolemic, AZ: azilsartan, I/R: ischemia-reperfusion, PostC: post-conditioning, L-NIO: selective eNOS inhibitor.

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  Fig. 5. Effect of azilsartan perfusion on (A) percent infarct size and (B) left ventricle collagen content in ischemia-reperfusion injury and ischemic-post conditioning of normal and hypercholesterolemic rats. Results are expressed as mean±standard deviation. ap<0.05 vs. sham control-NC group. bp<0.05 vs. I/R-NC group. cp<0.05 vs. sham control-HC group. dp<0.05 vs. I/R-HC group. ep<0.05 vs. AZ+PostC-I/R-HC group. NC: normocholesterolemic, HC: hypercholesterolemic, AZ: azilsartan, I/R: ischemia-reperfusion, PostC: post-conditioning, L-NIO: selective eNOS inhibitor.

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  Fig. 6. Effect of azilsartan perfusion on (A) TBARS, (B) SA and (C) GSH in ischemia-reperfusion injury and ischemic-post conditioning of normal and hypercholesterolemic rats. Results are expressed as mean±standard deviation. ap<0.05 vs. sham control–NC group. bp<0.05 vs. I/R–NC group. cp<0.05 vs. sham control–HC group. dp<0.05 vs. I/R–HC group. ep<0.05 vs. AZ+PostC-I/R–HC group. TBARS: thiobarbituric acid reactive substances, SA: superoxide anion, GSH: reduced form of the glutathione, NC: normocholesterolemic, HC: hypercholesterolemic, AZ: azilsartan, I/R: ischemia-reperfusion, PostC: post-conditioning, L-NIO: selective eNOS inhibitor.