Actividad inotrópica inducida por el derivado carbamacepina-alquino en un modelo de corazón aislado y perfundido a flujo constante

Introduction: Few data exist with respect to the effects of carbamazepine and its derivatives at cardiovascular level; furthermore, the molecular mechanisms and cellular site of action are still unclear. Objective: The effects induced by carbamazepine-alquine derivative on perfusion pressure, vascular resistance and left ventricular pressure were evaluated. Materials and methods: The effects of carbamazepine and carbamazepine-alquine on the perfusion pressure, vascular resistance and left ventricular pressure were examined in isolated rat hearts (Langendorff model). Results: Four results were obtained: (1) The carbamazepine-alquine derivative [10^-9 mM] increased the perfusion pressure and vascular resistance in comparison with the carbamazepine [10^-9 mM]; (2) the effect of carbamazepine-alquine derivative [10^-9-10^-4 mM] on left ventricular pressure not was inhibited by metoprolol or prazosin at a dose of 10-6 mM; (3) nifedipine [10^-6 mM] blocked the effects exerted by the carbamazepine-alquine derivative [10^-9-10^-4 mM] on left ventricular pressure, and (4) the carbamazepine-alquine derivative at dose of 10^-9 mM increased the concentration of intracellular calcium over a time period of 3-18 min; nevertheless, in presence of nifedipine [10^-6 mM] this effect was inhibited significantly (p=0.005). Conclusions: The activity exerted by carbamazepine-alquine derivative on perfusion pressure, vascular resistance and left ventricular pressure involved activation of calcium channel type-L, brought indirectly changes in the intracellular calcium levels and subsequently induced a positive inotropic effect.