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Nitric Oxide Metabolism after Traumatic Brain Injury

  • L. Rangel-Castilla
  • C. S. Robertson

Abstract

Nitric oxide (NO) is a cell membrane-permeable free radical gas and is the smallest known biologically active molecule. NO can be produced by nearly all tissues of the body. NO is synthesized from the semi-essential amino acid, L-arginine, by the enzyme, nitric oxide synthase (NOS). Three isoforms of NOS exist: Endothelial (eNOS), neuronal (nNOS), and inducible (iNOS). Agents that selectively inhibit the individual isoforms of NOS, as well as transgenic mice that are deficient in each of the isoforms of NOS, have played important roles in understanding the normal functions of NO and the changes in NO metabolism that occur with neurological disorders like traumatic brain injury (TBI) [1].

Keywords

Nitric Oxide Traumatic Brain Injury Cereb Blood Flow Fluid Percussion Injury Oxygenase Domain 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science + Business Media Inc. 2007

Authors and Affiliations

  • L. Rangel-Castilla
    • 1
  • C. S. Robertson
    • 2
  1. 1.Department of NeurosurgeryThe University of Texas MedicalGalvestonUSA
  2. 2.Department of NeurosurgeryBaylor College of MedicineHoustonUSA

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