%0 Journal Article
%T Inotropic activity induced by carbamazepine-alkyne derivative in an isolated heart model and perfused to constant flow Actividad inotr車pica inducida por el derivado carbamacepina-alquino en un modelo de coraz車n aislado y perfundido a flujo constante
%A Lauro Figueroa-Valverde
%A Francisco D赤az-Cedillo
%A Mar赤a L車pez-Ramos
%A Elodia Garc赤a-Cervera
%J Biom谷dica
%D 2011
%I Instituto Nacional de Salud
%X 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. Introducci車n. Existen pocos datos con respecto a los efectos de la carbamacepina y sus derivados en el aparato cardiovascular; adem芍s, el mecanismo molecular y su sitio de acci車n celular no son claros. Objetivo. Evaluar los efectos inducidos por el derivado carbamacepina-alquino sobre la presi車n de perfusi車n, la resistencia vascular y la presi車n ventricular izquierda. Materiales y m谷todos. Los efectos de la carbamacepina y del derivado carbamacepina-alquino sobre la presi車n de perfusi車n, la resistencia vascular y la presi車n ventricular izquierda fueron evaluados en un modelo de coraz車n aislado de rata (Langendorff). Resultados. Se encontr車 que: 1) el derivado carbamacepina-alquino (1x10-9 mM) incrementa la presi車n de perfusi車n y la resistencia vascular en comparaci車n con la carbamacepina (1℅10-9 mM); 2) los efectos del derivado carbamacepina-alquino (1℅10-9-1℅10-4 M) sobre la presi車n intraventricular no fueron inhibidos por metoprolol o prazosina (1℅10-6 mM); 3);
%K carbamacepina
%K nifedipino
%K presi車n ventricular
%K resistencia vascular
%K coraz車n
%U http://www.revistabiomedica.org/index.php/biomedica/article/view/310