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Nitroarginine Reduces Infarction After Middle Cerebral Artery Occlusion in Rats

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Abstract

Neuronal production of nitric oxide (·NO) provides a common link between two seemingly independent mechanisms of brain injury—excitatory neurotransmitters and oxygen radicals. The connection results from the recent demonstration that glutamate stimulates neurons to produce nitric oxide (Garthwaite et al. 1988). Neurons produce nitric oxide by oxidizing arginine with a calcium-activated enzyme that is physiologically activated by the N-methyl-D-asparate (NMDA) subclass of receptors (Garthwaite 1991). Neuronal nitric oxide helps regulate local cerebral blood flow, contributes in synaptic plasticity (Nowak 1992), and may have a role in the normal development of brain (Gaily et al. 1990). Ischemia and hypoxia initiate events that mimic the normal physiological regulation of the NMDA subclass of glutamate receptors, which may overproduce nitric oxide whentissue is reperfused. Oxidative metabolism disrupted by ischemia will produce the oxygen radical, superoxide (O2 ), that reacts with the elevated concentrations of nitric oxide to form the destructive species peroxynitrite (ONOO) and thereby exacerbating cerebral injury.

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© 1994 Springer-Verlag Berlin Heidelberg

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Chen, J., Conger, K.A., Tan, MJ., Beckman, J.S. (1994). Nitroarginine Reduces Infarction After Middle Cerebral Artery Occlusion in Rats. In: Hartmann, A., Yatsu, F., Kuschinsky, W. (eds) Cerebral Ischemia and Basic Mechanisms. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-78151-3_27

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  • DOI: https://doi.org/10.1007/978-3-642-78151-3_27

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-78153-7

  • Online ISBN: 978-3-642-78151-3

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