title: Response of spinal cord blood flow to the nitric oxide inhibitor nitroarginine.
abstract: OBJECTIVE
  The extent to which nitric oxide (NO) is involved in the modulation of spinal cord blood flow (SCBF) in the uninjured and injured cord is unknown. To elucidate these questions, the following experiments in anesthetized rats were conducted.
  
  
  METHODS
  Because NO is an unstable free radical with a half-life of seconds, its role can be understood through the study of the NO synthase inhibitor L-NG-nitroarginine (L-NOARG). L-NOARG was administered intravenously for 30 minutes at a dose of 100 or 500 micrograms/kg/min in 12 and 10 uninjured animals, respectively. SCBF fluctuations at C7-T1 were measured using laser doppler flowmetry. In a second set of 12 rats, L-NOARG (500 micrograms/kg/min) was administered 10 minutes before spinal cord injury using a modified aneurysm clip at C7-T1 and continued for 30 minutes thereafter.
  
  
  RESULTS
  In the uninjured animals, L-NOARG was associated with a dose-dependent increase in mean arterial pressure of 20 to 80% above baseline (P = 0.0001), together with a dose-related decrease in SCBF (P = 0.0373). In the injured animals, L-NOARG was associated with a 48% increase in mean arterial pressure. With L-NOARG, the changes in SCBF from baseline after injury were similar to those of noninjured controls (n = 25) and significantly less than injury controls (n = 18) or those receiving phenylephrine (n = 8).
  
  
  CONCLUSIONS
  NO synthase inhibitors, by reducing available NO, cause systemic vasoconstriction and a decrease in SCBF in the uninjured spinal cord. In the injured spinal cord, the administration of L-NOARG results in a redistribution of blood flow with an augmentation in posttraumatic SCBF at the injury site.
authors.affiliation: Department of Surgery, College of Medicine, University of Iowa, Iowa City, USA.
authors.forename: P W
authors.initials: PW
authors.lastname: Hitchon
authors.forename: L J
authors.initials: LJ
authors.lastname: Mouw
authors.forename: T N
authors.initials: TN
authors.lastname: Rogge
authors.forename: J C
authors.initials: JC
authors.lastname: Torner
authors.forename: A K
authors.initials: AK
authors.lastname: Miller
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D007262:Infusions, Intravenous; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000502:physiology; D019335:Nitroarginine / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013116:Spinal Cord / Q000098:blood supply*; D013119:Spinal Cord Injuries / Q000503:physiopathology
chemical_list: D019335:Nitroarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase