There are some reports which indicate that several triazole derivatives have inotropic activity; however, the cellular site and mechanism of action at cardiovascular level is very confusing. In order, to have a clear understanding of these phenomena, a triazole derivative was synthesized to evaluate its biological activity on left ventricular pressure and characterize the molecular mechanism. The Langendorff technique was used to measure changes on perfusion pressure and coronary resistance in an isolated rat heart model in absence or presence of the triazole derivative. Additionally, the molecular mechanism involved in the inotropic activity induced by the triazole derivative was evaluated by measuring left ventricular pressure in absence or presence of the following compounds; prazosin, metoprolol, nifedipine, indomethacin and the compound BM-531. The results showed that the triazole derivative significantly increased the perfusion pressure and coronary resistance in comparison with the control conditions. Other data indicate that the triazole derivative increase left ventricular pressure in a dose-dependent manner (0.001 to 100 nM); nevertheless, this phenomenon was significantly inhibited only by indomethacin and BM-531 at a dose of 1 nM. Therefore, experimental results suggest that positive inotropic activity induced by the triazole derivative is via activation of TXA2. This phenomenon is particularly interesting because the inotropic activity induced by the triazole derivative involves a molecular mechanism different in comparison with other positive inotropic drugs.