Central command dysfunction in rats with heart failure is mediated by brain oxidative stress and normalised by exercise training.

Koba S, Hisatome I, Watanabe T. J Physiol. 2014 Jun 27. The authors wanted to investigate the role of oxidative stress (OS) in the RVLM of rats with chronic heart failure (CHF) because it is believed that RVLM OS in CHF rats potentiates sympathoexcitation, and that this potentiation can be suppressed by exercise training. They then looked at the RNSA in CHF rats after an induced myocardial infarction (MI) and electrical stimulation of the mesencephalic locomotor region (MLR) compared to the same stimulation in controls and sham-MI CHF rats. The stimulation of the MLR was to simulate exercise training done in humans with MI and CHF, because many of these patients wind up with exercise intolerance due to the enhanced SNA. They found that injection of Tempol, which scavenges reactive oxygen species (ROS), in to the RVLM of control and CHF rats had no effect on RNSA following the stimulus, but did reduce the increased RNSA and MAP in MI CHF rats. They also stained the tissue with dihydroethidium to confirm that MI rats generated increased ROS as confirmation that they were actually seeing changes in ROS between groups specifically in the RVLM. What was interesting here was that their experiments were done after neuromuscular blockade, so this probably isn’t due to signals coming from the muscles, but may be due to collaterals coming from locomotor brain regions that project to RVLM or some area controlling it. Also, Mueller 2007 was referenced in this paper for its RVLM microinjection approach, so that’s cool. -DH