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Functional Characterization of Na+/H+ Exchangers of Intracellular Compartments Using Proton-killing Selection to Express Them at the Plasma Membrane
Published on: March 30, 2015
Papel del intercambiador Na(+) /H(+) en la remodelación electrofisiológica auricular a corto plazo
J V Jayachandran1, D P Zipes, J Weksler
1Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Circulation
|April 19, 2000
Resumen
La activación del intercambiador Na+/H+ (NHE, por sus siglas en inglés) contribuye a la remodelación electrofisiológica (ER, por sus siglas en inglés) de los ritmos auriculares rápidos. La inhibición de NHE previene la ER, preservando la función auricular durante el ritmo rápido y la isquemia.
Área de la Ciencia:
- Cardiología Cardiología.
- Electrofisiología y electrofisiología.
- Fisiología Celular Fisiología celular
Sus antecedentes:
- Los mecanismos de la remodelación electrofisiológica (ER) debido a los ritmos auriculares rápidos siguen sin estar claros.
- Este estudio investiga el papel del intercambiador Na+/H+ (NHE) en ER, con la hipótesis de que su activación por isquemia contribuye a este proceso.
Objetivo del estudio:
- Para determinar si la activación de NHE por isquemia contribuye a ER.
- Evaluar el efecto de la inhibición de NHE en la ER durante las tasas auriculares rápidas simuladas y la isquemia real.
Principales métodos:
- Veintiocho perros fueron estudiados bajo bloqueo autónomo.
- La fibrilación auricular se simuló mediante un ritmo auricular rápido (600 bpm durante 5 horas) en perros de pecho cerrado, y algunos recibieron un inhibidor selectivo de NHE (HOE642).
- La isquemia auricular derecha fue inducida en perros de pecho abierto, y algunos recibieron HOE642 o glibenclamida.
Principales resultados:
- En perros con ritmo, la inhibición de NHE impidió el acortamiento del período refractario efectivo auricular (AERP) y preservó la adaptación de la tasa.
- En perros con isquemia inducida, la inhibición de NHE impidió el acortamiento de la AERP y mantuvo la adaptación de la velocidad, a diferencia del tratamiento con glibenclamida.
- La inhibición de la NHE preservó con éxito las propiedades electrofisiológicas auriculares tanto en velocidades rápidas simuladas como en condiciones isquémicas.
Conclusiones:
- La activación del NHE es un mecanismo clave que impulsa la remodelación electrofisiológica a corto plazo.
- La inhibición del NHE puede prevenir cambios perjudiciales en la electrofisiología auricular causados por tasas rápidas e isquemia.
- Dirigirse a NHE puede ofrecer una estrategia terapéutica para manejar las arritmias auriculares y la remodelación relacionada.
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