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BioMed Research International
Volume 2014, Article ID 217865, 11 pages
Research Article

Activity Exerted by a Testosterone Derivative on Myocardial Injury Using an Ischemia/Reperfusion Model

1Laboratory of Pharmaco-Chemistry, Faculty of Chemical Biological Sciences, University Autonomous of Campeche, Avenida Agustín Melgar s/n, Colonia Buenavista, 24039 San Francisco de Campeche, CAM, Mexico
2Escuela Nacional de Ciencias Biológicas del Instituto Politéecnico Nacional, Prolongación de Carpio y Plan de Ayala s/n, Col. Santo Tomas, 11340 Mexico City, DF, Mexico
3Facultad de Nutrición, Médicos y Odontologos s/n, Unidad del Bosque, 91010 Xalapa, VER, Mexico
4Faculty of Medicine, University Autonomous of Campeche, Avenida Patricio Trueba de Regil s/n, Col Lindavista, 24090 San Francisco de Campeche, CAM, Mexico

Received 19 January 2014; Revised 4 March 2014; Accepted 5 March 2014; Published 16 April 2014

Academic Editor: Joen-Rong Sheu

Copyright © 2014 Figueroa-Valverde Lauro et al. 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.


Some reports indicate that several steroid derivatives have activity at cardiovascular level; nevertheless, there is scarce information about the activity exerted by the testosterone derivatives on cardiac injury caused by ischemia/reperfusion (I/R). Analyzing these data, in this study, a new testosterone derivative was synthetized with the objective of evaluating its effect on myocardial injury using an ischemia/reperfusion model. In addition, perfusion pressure and coronary resistance were evaluated in isolated rat hearts using the Langendorff technique. Additionally, molecular mechanism involved in the activity exerted by the testosterone derivative on perfusion pressure and coronary resistance was evaluated by measuring left ventricular pressure in the absence or presence of the following compounds: flutamide, prazosin, metoprolol, nifedipine, indomethacin, and PINANE TXA2. The results showed that the testosterone derivative significantly increases the perfusion pressure and coronary resistance in isolated heart. Other data indicate that the testosterone derivative increases left ventricular pressure in a dose-dependent manner (0.001–100 nM); however, this phenomenon was significantly inhibited by indomethacin and PINANE-TXA2   at a dose of 1 nM. In conclusion, these data suggest that testosterone derivative induces changes in the left ventricular pressure levels through thromboxane receptor activation.