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- W827340521 abstract "Background Ivabradine is a bradycardic agent, which inhibits the If-current in the sinus node. In pigs, ivabradine reduced infarct size even when given only at reperfusion and in the absence of heart rate reduction. Ivabradine´s protective action at reperfusion, when a burst of reactive oxygen species (ROS) is released, suggests it might attenuate ROS formation. Mitochondria are a major source of ROS after ischemia/reperfusion (I/R). Thus, we wanted to analyze a potential effect of ivabradine on mitochondrial function during simulated I/R. Methods: Mitochondria were isolated from C57Bl/6J mouse hearts and subjected to simulated I/R (6 min hypoxia/3 min normoxia) in glutamate/malate- and ADP-containing buffer ±3 µmol/l ivabradine at 30°C. After simulated I/R, mitochondrial complex I respiration (n=32,preparations), ROS concentration (n=9) and ATP production (n=15) were quantified. Results: After simulated I/R ivabradine did not affect mitochondrial complex I respiration, but reduced the ROS concentration (144±12 vs. 122±12 nmol H2O2/100 µg protein; p=0.01), and increased the ATP concentration (148±20 vs. 181±21 µmol/l; p=0.01). Conclusion Mitochondria seem to be a target of protection induced by ivabradine by reducing mitochondrial ROS formation and increasing mitochondrial ATP production. Further studies are necessary to identify such target structure/s of ivabradine on mitochondria." @default.
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- W827340521 date "2015-04-01" @default.
- W827340521 modified "2023-09-25" @default.
- W827340521 title "Mitochondria are a target of cardioprotection by ivabradine" @default.
- W827340521 doi "https://doi.org/10.1096/fasebj.29.1_supplement.954.6" @default.
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