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Effect of ryanodine on sinus node recovery time determined in vitro
J W Bassani1, C M Godoy, R A Bassani
1Centro de Engenharia Biomédica and Departamento de Engenharia Biomédica, Faculdade de Engenharia Elétrica e de Computação, Universidade Estadual de Campinas, Campinas, SP, Brasil. bassani@deb.fee.unicamp.br
Summary
Disabling the sarcoplasmic reticulum (SR) with ryanodine in rat atria did not affect basic atrial automaticity or conduction. However, it enhanced overdrive suppression of sinus node recovery time (SNRT) in a rate-dependent manner.
Area of Science:
- Cardiac Electrophysiology
- Cellular Physiology
- Pharmacology
Background:
- The sarcoplasmic reticulum (SR) is implicated in spontaneous electrical activity in atrial pacemaker cells.
- Understanding the SR's role is crucial for comprehending atrial automaticity and conduction disorders.
Purpose of the Study:
- To investigate the effect of inhibiting the SR with ryanodine on sinus node recovery time (SNRT) in isolated rat atria.
- To determine the SR's contribution to atrial automaticity, conduction, and overdrive suppression.
Main Methods:
- Isolated right atria from male Wistar rats were treated with ryanodine (0.1 microM).
- Electrograms and isometric force were recorded at 36.5°C.
- Sinus node resetting was achieved using single pulse or 2-minute train stimulation at varying coupling intervals; corrected SNRT (cSNRT) was calculated.
Main Results:
- Ryanodine slightly increased the regular cycle length (<10%) but reduced developed force by 90%.
- SR inhibition did not alter cSNRT when using the single pulse method, indicating preserved intranodal/atrial conduction.
- Ryanodine significantly prolonged cSNRT in a rate-dependent manner when using the train method, indicating enhanced overdrive suppression.
Conclusions:
- A functional SR is not essential for rat atrial automaticity, despite its importance for force development.
- Disruption of SR function and cellular calcium homeostasis does not impair cardiac conduction.
- Inhibition of SR function exacerbates overdrive-induced depression of sinusal automaticity.