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- Title
Actividad inotrópica inducida por el derivado carbamacepina-alquino en un modelo de corazón aislado y perfundido a flujo constante.
- Authors
Figueroa-Valverde, Lauro; Díaz-Cedillo, Francisco; López-Ramos, María; García-Cervera, Elodia; Quijano-Ascencio, Karen
- Abstract
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.
- Subjects
MYOCARDIAL depressants; CARBAMAZEPINE; CARDIOVASCULAR system; VENTRICULAR remodeling; MECHANICAL hearts
- Publication
Biomédica: Revista del Instituto Nacional de Salud, 2011, Vol 31, Issue 2, p232
- ISSN
0120-4157
- Publication type
Article
- DOI
10.7705/biomedica.v31i2.310