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Activity Induced by a Naphthalene-Prazosin Derivative on Ischemia/Reperfusion Injury in Rats

In this study, a new naphthalene-prazosin derivative (compound 5) was synthetized with the objective of evaluating its activity on ischemia/reperfusion injury. The Langendorff technique was used to evaluate the effect of the compound 5 on ischemia/reperfusion injury. Additionally, the mechanism of a...

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Bibliographic Details
Published in:Pharmacology & pharmacy 2014-11, Vol.5 (12), p.1130-1142
Main Authors: Sarabia-Alcocer, Betty, Figueroa-Valverde, Lauro, Díaz-Cedillo, Francisco, Hau-Heredia, Lenin, Rosas-Nexticapa, Marcela, García-Cervera, Elodia, Pool-Gómez, Eduardo, García-Martínez, Rolando, Zepeda-Acosta, Braulio
Format: Article
Language:English
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Summary:In this study, a new naphthalene-prazosin derivative (compound 5) was synthetized with the objective of evaluating its activity on ischemia/reperfusion injury. The Langendorff technique was used to evaluate the effect of the compound 5 on ischemia/reperfusion injury. Additionally, the mechanism of action involved in the activity exerted by the compound 5 on perfusion pressure and coronary resistance was evaluated by measuring left ventricular pressure in absence or presence of following compounds; prazosin, metoprolol, indomethacin and nifedipine. The results showed that the compound 5 reduced infarct size compared with the control conditions. Other results showed that the compound 5 significantly increases (p = 0.05) the perfusion pressure and coronary resistance in isolated rat heart. In addition, other data indicate that the compound 5 increases left ventricular pressure in a dose-dependent manner (0.001 to 100 nM); however, this phenomenon was significantly inhibited by nifedipine at a dose of 1 nM (p = 0.05) and this effect was independent of cAMP levels. In conclusion, these data suggest that the naphthalene-prazosin derivative exerts a cardio protective effect via the calcium channels activation and consequently induces changes in the left ventricular pressure levels. This phenomenon results in a decrease of myocardial necrosis after ischemia and reperfusion.
ISSN:2157-9423
2157-9431
DOI:10.4236/pp.2014.512123