scholarly journals Intracellular Calcium Dynamics, Shortened Action Potential Duration, and Late-Phase 3 Early Afterdepolarization in Langendorff-Perfused Rabbit Ventricles

2012 ◽  
Vol 23 (12) ◽  
pp. 1364-1371 ◽  
Author(s):  
LIANG TANG ◽  
BOYOUNG JOUNG ◽  
MASAHIRO OGAWA ◽  
PENG-SHENG CHEN ◽  
SHIEN-FONG LIN
Keyword(s):  
Action Potential ◽  
Intracellular Calcium ◽  
Action Potential Duration ◽  
Late Phase ◽  
Calcium Dynamics ◽  
Phase 3 ◽  
Early Afterdepolarization ◽  
Intracellular Calcium Dynamics

Modeling action potential generation and propagation in NRK fibroblasts

2004 ◽  
Vol 287 (4) ◽  
pp. C851-C865 ◽  
Author(s):  
J. J. Torres ◽  
L. N. Cornelisse ◽  
E. G. A. Harks ◽  
W. P. M. van Meerwijk ◽  
A. P. R. Theuvenet ◽  
...  
Keyword(s):  
Action Potential ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Cell Transformation ◽  
Rat Kidney ◽  
Potassium Conductance ◽  
Calcium Dynamics ◽  
Starting Point ◽  
Release Analysis ◽  
Intracellular Calcium Dynamics

Normal rat kidney (NRK) fibroblasts change their excitability properties through the various stages of cell proliferation. The present mathematical model has been developed to explain excitability of quiescent (serum deprived) NRK cells. It includes as cell membrane components, on the basis of patch-clamp experiments, an inwardly rectifying potassium conductance ( GKir), an L-type calcium conductance ( GCaL), a leak conductance ( Gleak), an intracellular calcium-activated chloride conductance [ GCl(Ca)], and a gap junctional conductance ( Ggj), coupling neighboring cells in a hexagonal pattern. This membrane model has been extended with simple intracellular calcium dynamics resulting from calcium entry via GCaL channels, intracellular buffering, and calcium extrusion. It reproduces excitability of single NRK cells and cell clusters and intercellular action potential (AP) propagation in NRK cell monolayers. Excitation can be evoked by electrical stimulation, external potassium-induced depolarization, or hormone-induced intracellular calcium release. Analysis shows the roles of the various ion channels in the ultralong (∼30 s) NRK cell AP and reveals the particular role of intracellular calcium dynamics in this AP. We support our earlier conclusion (De Roos A, Willems PH, van Zoelen EJ, and Theuvenet AP. Am J Physiol Cell Physiol 273: C1900–C1907, 1997) that AP generation and propagation may act as a rapid mechanism for the propagation of intracellular calcium waves, thus contributing to fast intercellular calcium signaling. The present model serves as a starting point to further analyze excitability changes during contact inhibition and cell transformation.

Intracellular calcium dynamics and cerebral injury: modeling various insults in vitro

1993 ◽  
Vol 613 (1) ◽  
pp. 156-159 ◽  
Author(s):  
Myung H. Kim-Lee ◽  
Bradford T. Stokes ◽  
Douglas K. Anderson
Keyword(s):  
Intracellular Calcium ◽  
Cerebral Injury ◽  
Calcium Dynamics ◽  
Intracellular Calcium Dynamics

scholarly journals Understanding anomalous delays in a model of intracellular calcium dynamics

2010 ◽  
Vol 20 (4) ◽  
pp. 045104 ◽  
Author(s):  
Emily Harvey ◽  
Vivien Kirk ◽  
Hinke M. Osinga ◽  
James Sneyd ◽  
Martin Wechselberger
Keyword(s):  
Intracellular Calcium ◽  
Calcium Dynamics ◽  
Intracellular Calcium Dynamics

Abstract 5328: Intracellular Calcium Mediated Late-Phase 3 Early Afterdepolarization Induces Ventricular Fibrillation in Isolated Rabbit Hearts with Activated K ATP Channel

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Liang Tang ◽  
Boyoung Joung ◽  
Juan Song ◽  
Masahiro Ogawa ◽  
Peng-Sheng Chen ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Intracellular Calcium ◽  
Single Cell ◽  
Transmembrane Potential ◽  
Optical Mapping ◽  
Late Phase ◽  
Acute Myocardial Ischemia ◽  
Phase 3 ◽  
Triggered Activity ◽  
Group I

Introduction: The mechanism and importance of late-phase 3 early after depolarization (EAD) in ventricular arrhythmogenesis and the corresponding intracellular calcium dynamics are unknown. Methods: We studied 22 Langendorff-perfused isolated normal rabbit hearts with and without K ATP channels opener, pinacidil (80 μM). In group I (n=10), we performed simultaneous dual optical mapping of transmembrane potential (V m ) and intracellular calcium (Ca i ) transient on left ventricular endocardium. In group II (n=6), glass microelectrode single cell recording of transmembrane potential (TMP) was performed. In group III (n=6), we examined the effects of BAPTA-AM, a calcium chelator, on late-phase 3 EAD and VF induction. Results: Ventricular endocardium was paced at PCL between 60 ms and 350 ms for 29 beats. Pinacidil shortened both APD 90 (192±11 ms at baseline to 98±9 ms) and duration of Ca i at 50% of amplitude (DCaT 50 , 152±10 ms at baseline to 84±9 ms) at PCL of 250 ms. At pacing rate < 200 ms, the first post-pacing spontaneous beat showed persistent APD shortening and late-phase 3 EAD accompanied by large Ca i elevation. There was a positive correlation between the EAD amplitudes and the amplitude of Ca i elevation (r=0.899). At a critical Ca i elevation magnitude, the late-phase 3 EAD then induced triggered activity and VF in 10 episodes. The single cell TMP recording confirmed the optical mapping data of late-phase 3 EAD-induced VF. Infusion of BAPTA-AM significantly reduced the maximal Ca i amplitude in the mapped region (26.4±3.5% of the control; p<0.001). Due to the lowered Ca i level, neither EAD in the first post-pacing beat nor VF induction was observed after pacing train at any PCLs. Conclusions: K ATP channel activation leads to shortened APD with correspondingly large Ca i elevation, resulting in late-phase 3 EAD in first spontaneous beat at the cessation of rapid pacing. Reducing intracellular calcium handling by BAPTA-AM prevented EAD and VF induction/reinitiation. Because acute myocardial ischemia activates the K ATP channel, the calcium mediated late-phase 3 EAD induced triggered activity may be a novel mechanism for VF and sudden death during acute myocardial ischemia. This research has received full or partial funding support from the American Heart Association, AHA National Center.

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