What question did this study set out to answer?

To investigate whether slow inward tail currents in rabbit ventricular and atrial myocytes are driven by electrogenic sodium-calcium exchange regulated by intracellular calcium release and uptake.

October 1, 1989The Journal of PhysiologyOpen Access

Slow inward tail currents in rabbit cardiac cells.

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Population

Single myocytes obtained by enzymatic dispersion of rabbit ventricle and atrium

Comparison

Various stimulation protocols, Tyrode solutions… vs Baseline or control conditions

Design

Preclinical

Authors

WGW GilesUniversity of Calgary YSY. ShimoniUniversity of Calgary

Discussion

Member takes

Implication

Hypothesis-generating for Na-Ca exchanger currents in arrhythmia models; leaves open translation to human electrophysiology.

Key Points

To investigate whether slow inward tail currents in rabbit ventricular and atrial myocytes are driven by electrogenic sodium-calcium exchange regulated by intracellular calcium release and uptake.
Applied whole-cell gigaseal suction microelectrode voltage-clamp techniques to single enzymatically dispersed rabbit ventricular and atrial myocytes.
Tested activation and decay dynamics using varying depolarization pulse durations (10 to 200 ms) and thermal shifts.
Manipulated ionic environments and transport via strophanthidin (10⁻⁵ M), reduced extracellular potassium (0.5 mM), elevated extracellular potassium (10-15 mM), and substitution with barium chloride or strontium chloride.
Tail currents activated with pulses as short as 10 ms, maximized at durations of 100-200 ms, and decayed faster following longer activating depolarizations, ruling out calcium current deactivation.
Elevating intracellular calcium via sodium-potassium pump inhibition (strophanthidin or 0.5 mM extracellular potassium) significantly enhanced tail current amplitude prior to contracture onset.
Tail currents were markedly reduced and decayed slower upon barium substitution (0.5-2.2 mM) or elevation of extracellular potassium to 10-15 mM, while remaining unchanged under strontium replacement (2.2 mM).

Structured PICO

Population

Single myocytes obtained by enzymatic dispersion of rabbit ventricle and atrium

Intervention

Various stimulation protocols, Tyrode solutions, and pharmacological agents (e.g., strophanthidin, BaCl2, SrCl2, varying [K+]o, temperature changes)

Comparator

Baseline or control conditions (e.g., standard Tyrode solution, normal [Ca2+]o)

Outcome

Characteristics and modulation of slow inward tail currents (activation, decay rate, dependence on [Ca2+]i, [K+]o, temperature, and inhibition by BaCl2)surrogate

This preclinical study characterizes slow inward tail currents in rabbit cardiac myocytes, providing evidence that they are generated by an electrogenic Na(+)-Ca2+ exchanger modulated by intracellular calcium and sarcoplasmic reticulum uptake.

Cite This Study

Giles et al. (1989) studied this question.

synapsesocial.com/papers/6a8a87d10e1a8f7244fd808e https://doi.org/10.1113/jphysiol.1989.sp017812

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Slow inward tail currents in rabbit cardiac cells.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Slow inward tail currents in rabbit cardiac cells.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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