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Underlying mechanism for prolongation of action potential duration in ventricular cardiomyocytes of rats suffered from thermal injury / 生理学报
Acta Physiologica Sinica ; (6): 375-381, 2007.
Artigo em Chinês | WPRIM | ID: wpr-258641
ABSTRACT
Severe thermal injury causes prolongation of action potential duration (APD) in cardiomyocytes, which results in cardiac dysfunction by inducing disturbance of calcium dyshomeostasis in cardiac myocytes. However, the underlying mechanism for APD prolongation remains unclear. In the present study, we examined the major action potential repolarization-related ion channel currents in rat ventricular cardiomyocytes, including transient outward potassium current (I(to)), inward rectifier potassium current (I(K1)) and L-type Ca(2+) current (I(Ca-L)) to investigate the alterations of these currents, which might account for the pathogenesis of APD prolongation induced by thermal injury. Twelve hours after approximately 40% of the total body surface area, full-thickness (third-degree) cutaneous thermal injury was produced in rats, ventricular cardiomyocytes were isolated from the hearts with systolic and diastolic dysfunction. APD was found to be markedly prolonged, while APD(50) and APD(90) in ventricular cardiomyocytes from rats with thermal injury were (46.02+/-3.78) ms and (123.24+/-12.48) ms (n=19), respectively, significantly longer than (23.28+/-4.85) ms and (72.12+/-3.57) ms (n=17, P<0.01) in ventricular cardiomyocytes from sham rats. Thermal injury remarkably suppressed Ito density in ventricular cardiomyocytes. Ito density at +60 mV was decreased from (34.15+/-3.78) pA/pF (n=20) in sham group to (20.39+/-1.98) pA/pF (n=25, P<0.01) in thermal injury group, and the decrease extended from -30 to +60 mV. Similarly, current densities of I(K1) from -120 to -80 mV in thermal injury group were also significantly lower than that in sham group. In contrast, we failed to detect any alterations in I(Ca-L) density, and voltage-dependence of activation and inactivation in thermal injury group, compared with that in sham group. Taken together, our data suggest that thermal injury results in function downregulation of transient outward potassium channels and inward rectifier potassium channels, which contributes, at least in part, to APD prolongation and subsequent cardiac dysfunction.
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Fisiologia / Fatores de Tempo / Potenciais de Ação / Queimaduras / Função Ventricular / Ratos Sprague-Dawley / Canais de Cálcio Tipo L / Canais de Potássio Corretores do Fluxo de Internalização / Miócitos Cardíacos Limite: Animais Idioma: Chinês Revista: Acta Physiologica Sinica Ano de publicação: 2007 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Fisiologia / Fatores de Tempo / Potenciais de Ação / Queimaduras / Função Ventricular / Ratos Sprague-Dawley / Canais de Cálcio Tipo L / Canais de Potássio Corretores do Fluxo de Internalização / Miócitos Cardíacos Limite: Animais Idioma: Chinês Revista: Acta Physiologica Sinica Ano de publicação: 2007 Tipo de documento: Artigo