Potassium channel blockade amplifies cardiac instability numerical studies of torsades de pointes.
Indian J Physiol Pharmacol
;
1994 Oct; 38(4): 259-66
Artículo
en Inglés
| IMSEAR
| ID: sea-107665
ABSTRACT
Suppression of responses to premature stimulation has been the guiding principle in managing many cardiac arrhythmias. Recent clinical trails revealed that sodium channel blockade increased the incidence of re-entrant cardiac arrhythmias resulting in sudden cardiac death, although the physiologic mechanism remains uncertain. Potassium channel blockade offers an alternative mechanism for suppressing responses to premature stimuli. We have developed a simple model of a 2D sheet of excitable cells. We can initiate re-entrant activation with stimuli timed to occur within a period of vulnerability (VP). Reducing the Na conductance increases the VP while reducing the K conductance increases the collective instability of the array, and arrhythmias similar to torsades de pointes seen in patients subjected to K channel blocked can be readily initiated. Thus, while K channel blockade may suppress excitability by prolonging the action potential duration, it appears to simultaneously exhibit proarrhythmic properties that result in complex re-entrant arrhythmias.
Texto completo:
Disponible
Índice:
IMSEAR (Asia Sudoriental)
Asunto principal:
Arritmia Sinusal
/
Biofisica
/
Potenciales de Acción
/
Humanos
/
Canales de Potasio
/
Canales de Sodio
/
Torsades de Pointes
/
Muerte Súbita Cardíaca
/
Bloqueadores de los Canales de Potasio
/
Bloqueadores de los Canales de Sodio
Idioma:
Inglés
Revista:
Indian J Physiol Pharmacol
Año:
1994
Tipo del documento:
Artículo
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