title: Spinal cord infarcts during long-term inhibition of nitric oxide synthase in rats.
abstract: OBJECTIVE
  Chronic hypertension is a major predisposing factor for stroke in humans. It has recently been shown that long-term inhibition of nitric oxide synthase activity causes a gradual time-dependent increase in arterial blood pressure in rats. We used this new animal model of chronic hypertension to study the occurrence and spatial features of infarcts in the central nervous system.
  
  
  METHODS
  Rats were treated with a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester, dissolved in the drinking water at 50 mg/kg per day for 11 weeks. The brains and spinal cords of hypertensive rats with and without motion disturbances were processed for standard microscopic examination.
  
  
  RESULTS
  Seventy-nine percent of the hypertensive rats showed motion dysfunctions, especially front leg paralysis, and/or died suddenly when their systolic blood pressure reached approximately 215 mm Hg after approximately 7 weeks of treatment. All of the hypertensive rats with stroke had spinal cord infarcts (90% at the cervical or cervicothoracic level) either alone or combined with brain lesions (30%). These structural alterations ranged from focal areas of pale, spongy tissue to large necrotic sites with vascular alterations, including thickened or fibrinoid degenerated vessel wall, macrophage invasion, and reactive astrocytes.
  
  
  CONCLUSIONS
  Infarcts occurred in the central nervous system with a high incidence in the spinal cord of hypertensive rats in which nitric oxide synthase was chronically blocked. This location of the hypertensive neuropathologic sequelae contrasts with the model of stroke-prone spontaneously hypertensive rats. The results suggest that nitric oxide is a key factor in spinal cord arteriolar vasomotion and structure in rats.
authors.affiliation: Ecole Vétérinaire d'Alfort, Maisons-Alfort, France.
authors.forename: S
authors.initials: S
authors.lastname: Blot
authors.forename: J F
authors.initials: JF
authors.lastname: Arnal
authors.forename: Y
authors.initials: Y
authors.lastname: Xu
authors.forename: F
authors.initials: F
authors.lastname: Gray
authors.forename: J B
authors.initials: JB
authors.lastname: Michel
mesh_terms: D000594:Amino Acid Oxidoreductases / Q000037:antagonists & inhibitors*; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives*; D001158:Arteries / Q000473:pathology; D001921:Brain / Q000473:pathology; D006973:Hypertension / Q000139:chemically induced / Q000150:complications / Q000503:physiopathology*; D007238:Infarction / Q000209:etiology* / Q000473:pathology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000037:antagonists & inhibitors*; D019001:Nitric Oxide Synthase; D051381:Rats; D013116:Spinal Cord / Q000098:blood supply* / Q000473:pathology
chemical_list: D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases; D019331:NG-Nitroarginine Methyl Ester