2002
Arrhythmogenic effect of extracellular K-depletion is prevented by the transverse-axial tubular system in a ventricular cardiac cell model
PÁSEK, Michal, Georges CHRISTÉ a Jiří ŠIMURDAZákladní údaje
Originální název
Arrhythmogenic effect of extracellular K-depletion is prevented by the transverse-axial tubular system in a ventricular cardiac cell model
Autoři
PÁSEK, Michal (203 Česká republika, garant), Georges CHRISTÉ (250 Francie) a Jiří ŠIMURDA (203 Česká republika)
Vydání
Scripta Medica Fac.Med.Univ.Masaryk.Brun. Brno, Faculty of Medicine, Masaryk University, 2002, 1211-3395
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30105 Physiology
Stát vydavatele
Česká republika
Utajení
není předmětem státního či obchodního tajemství
Kód RIV
RIV/00216224:14110/02:00007136
Organizační jednotka
Lékařská fakulta
Klíčová slova anglicky
ventricular cell; low external [K]; tubular system; quantitative modelling
Změněno: 6. 11. 2003 16:46, doc. Ing. Michal Pásek, Ph.D.
Anotace
V originále
In this work, we studied the role of the transverse-axial tubular system (TAT-system) in arrythmogenesis of ventricular cardiac cells under conditions of simulated hypokalaemia (low [K]e). We used the model of a mammalian ventricular myocyte that integrated the quantitative description of electrical activity of surface and tubular membranes and dynamic changes in intracellular ion concentrations. To maintain potassium homeostasis, an energy-dependent K+ extrusion pump was incorporated into the model. According to predictions provided by the model, the TAT-system protects the cell against arrhythmogenesis due to the enhancement of a potassium concentration gradient between tubular and extracellular spaces at low levels of [K]e. The energy-dependent K extrusion pump maintains tubular [K] at a level higher than the overall [K]e. This makes the activation of tubular K-conductances responsible for action potential repolarisation and resting voltage.
Návaznosti
GP204/02/D129, projekt VaV |
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