Abstract
Background: Intravenous amiodarone has increasingly been used to control life-threatening atrial and ventricular arrhythmias. In addition to its four antiarrhythmic properties, amiodarone may have complex effects on intracellular Ca2+ stores and myocyte contractility. Methods and Results: Contraction amplitude was recorded for cardiac ventricular myocytes isolated from neonatal and adult rabbits. Sarcoplasmic reticulum (SR) Ca2+ stores were loaded to steady-state levels by a train of eight electric field stimulations. The SR Ca2+ load was quantified by recording the contraction amplitude resulting from the complete depletion of SR Ca2+ stores by exposing the cell to a 1-second pulse of 10 mmol/L caffeine. After the cells were exposed to 1 μmol/L amiodarone for 10 minutes, electrically stimulated contraction amplitudes significantly decreased in both adult and neonatal cells. Caffeine-induced cell contraction amplitudes were not affected by amiodarone in adult ventricular myocytes. By contrast, amiodarone markedly inhibited caffeine-induced contractions in neonatal ventricular myocytes. The inhibitory effect of amiodarone on the caffeine-induced contractions was not replicated by Ca2+ channel blockade with diltiazem. Conclusions: Amiodarone markedly inhibits caffeine-induced contraction in neonatal myocytes but has no significant effect on adult myocytes. Ca2+ influx through amiodarone- sensitive Ca2+ channels may play a primary role in maintaining SR Ca2+ stores in neonatal heart.
Original language | English (US) |
---|---|
Pages (from-to) | 23-32 |
Number of pages | 10 |
Journal | Journal of Cardiovascular Pharmacology and Therapeutics |
Volume | 4 |
Issue number | 1 |
DOIs | |
State | Published - 1999 |
Externally published | Yes |
Keywords
- Amiodarone
- Antiarrhythmic agent
- Arrhythmia
- Ca channel blocker
- Excitation- contraction coupling
- Neonatal heart
ASJC Scopus subject areas
- Pharmacology
- Cardiology and Cardiovascular Medicine
- Pharmacology (medical)