Monosialoganglioside GM1 inhibits neurotoxicity after hypothermic circulatory arrest.

@article{Tseng1998MonosialogangliosideGI,
  title={Monosialoganglioside GM1 inhibits neurotoxicity after hypothermic circulatory arrest.},
  author={Elaine E. Tseng and Malcolm V. Brock and Mary S Lange and Juan C Troncoso and Mary E. Blue and Charles J Lowenstein and Michael V Johnston and William A. Baumgartner},
  journal={Surgery},
  year={1998},
  volume={124 2},
  pages={298-306}
}
BACKGROUND Prolonged hypothermic circulatory arrest (HCA) causes clinical neurologic injury. This injury involves neuronal apoptosis, or programmed cell death. We have previously demonstrated that HCA causes glutamate excitotoxicity, increased nitric oxide (NO) production, and NO-mediated apoptosis. We hypothesized that monosialoganglioside GM1 inhibits NO synthase. The purpose of this study was to determine whether GM1 inhibits NO production and neuronal apoptosis after HCA. METHODS Fourteen… CONTINUE READING

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