Opposite effects of halothane on guinea-pig ventricular action potential duration

2000 ◽  
Vol 390 (1-2) ◽  
pp. 95-101 ◽  
Author(s):  
Cécile Terrenoire ◽  
Vincent Piriou ◽  
Robert Bonvallet ◽  
Christophe Chouabe ◽  
Leon Espinosa ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potential Duration ◽  
Ventricular Action Potential

Dual effects of external magnesium on action potential duration in guinea pig ventricular myocytes

1995 ◽  
Vol 268 (6) ◽  
pp. H2321-H2328 ◽  
Author(s):  
S. Zhang ◽  
T. Sawanobori ◽  
H. Adaniya ◽  
Y. Hirano ◽  
M. Hiraoka
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Decay Time ◽  
Action Potential Duration ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Membrane Surface ◽  
Surface Charges ◽  
Whole Cell Patch Clamp ◽  
K Current

Effects of extracellular magnesium (Mg2+) on action potential duration (APD) and underlying membrane currents in guinea pig ventricular myocytes were studied by using the whole cell patch-clamp method. Increasing external Mg2+ concentration [Mg2+]o) from 0.5 to 3 mM produced a prolongation of APD at 90% repolarization (APD90), whereas 5 and 10 mM Mg2+ shortened it. [Mg2+]o, at 3 mM or higher, suppressed the delayed outward K+ current and the inward rectifier K+ current. Increases in [Mg2+]o depressed the peak amplitude and delayed the decay time course of the Ca2+ current (ICa), the latter effect is probably due to the decrease in Ca(2+)-induced inactivation. Thus 3 mM Mg2+ suppressed the peak ICa but increased the late ICa amplitude at the end of a 200-ms depolarization pulse, whereas 10 mM Mg2+ suppressed both components. Application of 10 mM Mg2+ shifted the voltage-dependent activation and inactivation by approximately 10 mV to more positive voltage due to screening the membrane surface charges. Application of manganese (1-5 mM) also caused dual effects on APD90, similar to those of Mg2+, and suppressed the peak ICa with slowed decay. These results suggest that the dual effects of Mg2+ on APD in guinea pig ventricular myocytes can be, at least in part, explained by its action on ICa with slowed decay time course in addition to suppressive effects on K+ currents.

Action potential duration and force-frequency relationship in isolated rabbit, guinea pig and rat cardiac muscle

1996 ◽  
Vol 166 (2) ◽  
pp. 150-155 ◽  
Author(s):  
P. Szigligeti ◽  
C. Pankucsi ◽  
T. B�ny�sz ◽  
A. Varr� ◽  
P. P. N�n�si
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Cardiac Muscle ◽  
Action Potential Duration ◽  
Force Frequency ◽  
Frequency Relationship

scholarly journals Inhibition of HERG K + Current and Prolongation of the Guinea‐Pig Ventricular Action Potential by 4‐Aminopyridine

2003 ◽  
Vol 549 (3) ◽  
pp. 667-672 ◽  
Author(s):  
J. M. Ridley ◽  
J. T. Milnes ◽  
Y. H. Zhang ◽  
H. J. Witchel ◽  
J. C. Hancox
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
K Current ◽  
Ventricular Action Potential

Electrotonic interactions in delayed propagation and block within the guinea pig SA node

1983 ◽  
Vol 245 (1) ◽  
pp. H7-H16 ◽  
Author(s):  
S. L. Lipsius
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potential Duration ◽  
Progressive Increase ◽  
Pacemaker Cells ◽  
Sa Node ◽  
Transmembrane Potentials ◽  
Electrotonic Interactions ◽  
Rapid Pacing ◽  
Exit Block

The influence of electrotonic interactions on propagation within the SA node was studied by recording transmembrane potentials simultaneously from two neighboring (less than 1 mm apart) subsidiary pacemaker cells within the sinoatrial (SA) node of the guinea pig. As single premature stimuli were delivered progressively earlier in diastole, retrograde propagation between cells was delayed progressively. Cells activated earlier displayed secondary depolarizations that were coincident with the depolarization of neighboring cells activated later. The secondary depolarizations increased action potential duration markedly. Rapid pacing elicited secondary depolarizations that resulted in a progressive increase in action potential duration and decrease in upstroke amplitude. These changes were associated with a progressive delay in retrograde propagation that led to intermittent block with Wenckebach periodicity. Exposure to tetrodotoxin (10(-5) g/ml) delayed antegrade propagation, resulting in electrotonically mediated secondary depolarizations and exit block with Wenckebach periodicity. It is concluded that delayed activation and electrotonically mediated interactions between cells can increase action potential duration and refractoriness. These changes contribute to progressive delays in propagation that may result in intermittent block with Wenckebach periodicity within the SA node.

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