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Electrical decoupling by Sr action potentials in guinea-pig papillary muscle
Pflugers Archiv : European Journal of Physiology
|September 1, 1982
Summary
Strontium (Sr2+) exposure in guinea-pig papillary muscle increases longitudinal resistance (ri) and slows conduction velocity. This effect is reversible with sodium (Na+) and linked to junctional decoupling, impacting muscle contraction and relaxation.
Area of Science:
- Cardiac Electrophysiology
- Membrane Biophysics
- Muscle Physiology
Background:
- Understanding cardiac muscle electrophysiology is crucial for diagnosing and treating heart conditions.
- Membrane constants, such as longitudinal resistance, are key determinants of cardiac action potential propagation.
- The role of specific ions like strontium (Sr2+) in modulating these constants requires further investigation.
Purpose of the Study:
- To investigate the impact of strontium (Sr2+) on the membrane constants of guinea-pig papillary muscle.
- To analyze the relationship between changes in longitudinal resistance (ri) and action potential conduction velocity.
- To explore the underlying mechanisms of Sr2+-induced electrophysiological alterations.
Main Methods:
- Cable analysis of guinea-pig papillary muscle.
- Utilized a single sucrose gap and micro-electrode recordings.
- Performed perfusions with Na-free and Na-containing Sr Tyrode solutions.
Main Results:
- In Na-free 20 mmol/l Sr Tyrode, longitudinal resistance (ri) increased by 210% (10 action potentials) and 457% (20 action potentials).
- This increase in ri was reversible upon perfusion with Na-containing solutions and absent in Na-containing Sr Tyrode.
- Conduction velocity decreased from 8.6 to 3.1 cm/s, and muscle relaxation slowed significantly in Na-free Sr Tyrode.
Conclusions:
- Sr2+ significantly increases longitudinal resistance (ri) in cardiac muscle, likely due to junctional decoupling.
- The observed increase in ri is associated with reduced action potential conduction velocity and impaired muscle relaxation.
- Junctional decoupling may result from intracellular Sr2+ accumulation or increased intracellular H+.