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The phosphodiesterase-5 inhibitor tadalafil reduces myocardial infarct size.

Authors: C Sesti|||V Florio|||E G Johnson|||R A Kloner

Journal: International journal of impotence research

Publication Type: Journal Article

Date: 2007

DOI: 10.1038/sj.ijir.3901497

ID: 16858368

Affiliations:

Affiliations

    Department of Medicine, The Heart Institute, Keck School of Medicine, University of Southern California, Good Samaritan Hospital, Los Angeles, CA 90017-2395, USA.|||||||||

Abstract

The aim of this study was to determine, in an animal model, the effects of tadalafil on myocardial infarct size (IS), hemodynamics and regional myocardial blood flow after myocardial ischemia and reperfusion. Patients with erectile dysfunction (ED) often have risk factors for coronary artery disease. Tadalafil, a long-acting inhibitor of the enzyme phosphodiesterase-5 (PDE5), is used for the treatment of ED; there are no previous data regarding tadalafil in the setting of coronary artery occlusion (CAO). Sprague-Dawley male rats were treated with tadalafil or vehicle (10 mg/kg, by gastric gavage), 2 h before a 30 min CAO. Heart rate was comparable between tadalafil and control groups. Tadalafil reduced mean arterial pressure (P=0.009), systolic (P=0.035) and diastolic (P=0.009) blood pressures during ischemia/reperfusion. Tadalafil significantly reduced IS (42+/-2%) versus controls (54+/-3%) (P=0.006). For the first time, we showed that the PDE5 inhibitor, tadalafil, was well tolerated and cardioprotective in the setting of an experimental myocardial infarction, by substantially reducing ischemic cell death.


Chemical List

    Carbolines|||Phosphodiesterase Inhibitors|||Potassium Channels|||Tadalafil