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NAC changes the course of cerebral small vessel disease in SHRSP and reveals new insights for the meaning of stases - a randomized controlled study.

Celine Zoe BuecheCornelia GarzSiegfried KropfDaniel BittnerWenjie LiMichael GoertlerHans-Jochen HeinzeKlaus ReymannHolger BraunStefanie Schreiber
Published in: Experimental & translational stroke medicine (2013)
NAC reduces the frequency of thromboses and infarcts to the expense of an increase of small microbleeds in a rat model of microangiopathic cerebrovascular disease. We suppose that NAC acts via an at least partial inactivation of vWF resulting in an insufficient sealing of initial endothelial injury leading to more small microbleeds. By elevating Glutathione-levels NAC most likely exerts a radical scavenger function and protects small vessels against extended ruptures and subsequent infarcts. Finally, it reveals that stases are mainly caused by endothelial injuries and restricted thromboses.
Keyphrases
  • transcription factor
  • endothelial cells
  • genome wide analysis