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Int. J. Mol. Sci. 2015, 16(11), 27015-27031; doi:10.3390/ijms161126010

Sildenafil Protects against Myocardial Ischemia-Reperfusion Injury Following Cardiac Arrest in a Porcine Model: Possible Role of the Renin-Angiotensin System

1
Department of Emergency Medicine, Beijing Chao-Yang Hospital, Capital Medical University, 8# Worker’s Stadium South Road, Chao-Yang District, Beijing 100020, China
2
Department of Emergency Medicine, Beijing Friendship Hospital, Capital Medical University, 95# Yong’an Road, Xicheng District, Beijing 100050, China
*
Author to whom correspondence should be addressed.
Academic Editor: Cesar Borlongan
Received: 22 August 2015 / Revised: 13 October 2015 / Accepted: 3 November 2015 / Published: 12 November 2015
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

Sildenafil, a phosphodiesterase-5 inhibitor sold as Viagra, is a cardioprotector against myocardial ischemia/reperfusion (I/R) injury. Our study explored whether sildenafil protects against I/R-induced damage in a porcine cardiac arrest and resuscitation (CAR) model via modulating the renin-angiotensin system. Male pigs were randomly divided to three groups: Sham group, Saline group, and sildenafil (0.5 mg/kg) group. Thirty min after drug infusion, ventricular fibrillation (8 min) and cardiopulmonary resuscitation (up to 30 min) was conducted in these animals. We found that sildenafil ameliorated the reduced cardiac function and improved the 24-h survival rate in this model. Sildenafil partly attenuated the increases of plasma angiotensin II (Ang II) and Ang (1–7) levels after CAR. Sildenafil also decreased apoptosis and Ang II expression in myocardium. The increases of expression of angiotensin-converting-enzyme (ACE), ACE2, Ang II type 1 receptor (AT1R), and the Ang (1–7) receptor Mas in myocardial tissue were enhanced after CAR. Sildenafil suppressed AT1R up-regulation, but had no effect on ACE, ACE2, and Mas expression. Sildenafilfurther boosted the upregulation of endothelial nitric oxide synthase (eNOS), cyclic guanosine monophosphate (cGMP) and inducible nitric oxide synthase(iNOS). Collectively, our results suggest that cardioprotection of sildenafil in CAR model is accompanied by an inhibition of Ang II-AT1R axis activation. View Full-Text
Keywords: sildenafil; myocardial ischemia; renin-angiotensin system; porcine model; Ang (1–7) sildenafil; myocardial ischemia; renin-angiotensin system; porcine model; Ang (1–7)
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Wang, G.; Zhang, Q.; Yuan, W.; Wu, J.; Li, C. Sildenafil Protects against Myocardial Ischemia-Reperfusion Injury Following Cardiac Arrest in a Porcine Model: Possible Role of the Renin-Angiotensin System. Int. J. Mol. Sci. 2015, 16, 27015-27031.

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