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Action potential and contractility changes in [Na(+)](i) overloaded cardiac myocytes: a simulation study.
1Cardiac Bioelectricity Research and Training Center and Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio 44106-7207 USA.
Biophysical Journal
|April 25, 2000
Summary
Elevated intracellular sodium in cardiac cells shortens action potential duration (APD) and increases intracellular calcium, promoting fatal arrhythmias. This study reveals sodium overload
Area of Science:
- Cardiovascular Physiology
- Computational Biology
- Cardiac Electrophysiology
Background:
- Sodium overload in cardiac cells is linked to pathologies and fatal arrhythmias.
- Understanding the impact of intracellular sodium on cardiac function is crucial for arrhythmia research.
Purpose of the Study:
- To investigate the effects of elevated intracellular sodium on the cardiac action potential (AP) and intracellular calcium.
- To elucidate the mechanisms underlying sodium-induced changes in cardiac electrophysiology using the Luo-Rudy model.
Main Methods:
- Utilized the Luo-Rudy computational model of a mammalian ventricular myocyte.
- Simulated conditions of elevated intracellular sodium concentration ([Na(+)](i)) and rapid pacing.
Main Results:
- Action potential duration (APD) shortened in two phases: a rapid phase due to I(Ks) accumulation and a slower phase driven by I(NaK) and reverse-mode I(NaCa).
- Sodium overload slowed AP depolarization, enhanced calcium influx via I(Ca(L)) and reverse-mode I(NaCa), leading to increased intracellular calcium transients.
- Reverse-mode I(NaCa) was identified as a trigger for calcium release, dependent on voltage and [Na(+)](i).
Conclusions:
- Sodium overload enhances the inducibility of reentrant arrhythmias by slowing AP depolarization and shortening APD.
- Shortened APD coupled with elevated intracellular calcium predisposes the myocardium to arrhythmogenic delayed afterdepolarizations.