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Transient outward current modulates discontinuous conduction in rabbit ventricular cell pairs
D J Huelsing1, A E Pollard, K W Spitzer
1Cardiac Rhythm Management Lab and Department of Biomedical Engineering, University of Alabama-Birmingham, Volker Hall B140, 1670 University Blvd., Birmingham, AL 35294, USA. djh@crml.uab.edu
Cardiovascular Research
|March 7, 2001
Summary
Inhibiting the transient outward current (I(to)) significantly improved conduction between heart cells, even under challenging conditions. This suggests I(to) plays a role in abnormal heart rhythms related to heart rate.
Area of Science:
- Cardiovascular Physiology
- Electrophysiology
- Cellular Biology
Background:
- The L-type calcium current is known to influence cardiac conduction.
- The role of the transient outward current (I(to)) in cardiac conduction is not well understood.
Purpose of the Study:
- To investigate the impact of inhibiting the transient outward current (I(to)) on conduction between ventricular myocytes.
- To determine if I(to) contributes to conduction abnormalities.
Main Methods:
- Electrically coupled single epicardial myocytes from rabbit right ventricle using a variable resistance circuit.
- Inhibited I(to) using 4-aminopyridine, rate-acceleration, and premature stimulation.
- Assessed effects on conduction delay and critical junctional resistance (R(j)).
Main Results:
- I(to) inhibition enhanced conduction, decreasing conduction delay by 32-41% and increasing critical R(j) by 36-73%.
- Pharmacologic inhibition, rate acceleration, and premature stimulation all demonstrated significant improvements in conduction.
- Premature action potentials showed the most pronounced effect, with shorter conduction delay and higher critical R(j).
Conclusions:
- Transient outward current (I(to)) inhibition significantly improves conduction, particularly across high junctional resistance.
- These findings indicate that I(to) may contribute to rate-dependent conduction abnormalities in the heart.