Reperfusion damage following focal ischemia: pathophysiology and therapeutic windows.

@article{Kuroda1997ReperfusionDF,
  title={Reperfusion damage following focal ischemia: pathophysiology and therapeutic windows.},
  author={Satoshi Kuroda and Bo K. Siesj{\"o}},
  journal={Clinical neuroscience},
  year={1997},
  volume={4 4},
  pages={199-212}
}
The mechanisms of reperfusion damage following focal cerebral ischemia are not known in detail. Recent results, however, strongly suggest that reactive oxygen species (ROS), generated during the reperfusion period, may trigger the reperfusion injury. Mitochondrial calcium overload and a permeability transition (PT) of the inner mitochondrial membrane have been shown to play an important role in production of ROS by the mitochondria. The immunosuppressant cyclosporin A (CsA), which inhibits… CONTINUE READING