title: Cyclosporin A reduces delayed motor neuron death after spinal cord ischemia in rabbits.
abstract: BACKGROUND
  Spinal cord ischemia has varied etiologies, and in some cases, may develop into paraplegia. This is attributable to the vulnerability of spinal motor neurons to ischemia. We evaluated the potential of the immunosuppressant cyclosporin A for treatment of spinal motor neuron damage caused by ischemia.
  
  
  METHODS
  Twenty-eight rabbits were randomized into four groups of 7 animals each: group A (cyclosporin A not administered), group B (2.5 mg/kg cyclosporin A), group C (25 mg/kg cyclosporin A), and group S (sham-operated). The spinal cord ischemia model was created by a 15-minute occlusion of the aorta just caudal to a renal artery with a balloon catheter. Administration of cyclosporin A began 30 minutes after restoration of blood flow. The spinal cords were removed after 7-day monitoring of neurologic function. Pathology specimens were prepared, and after staining them with hematoxylin-eosin, viable motor neurons in the ventral spinal cord were counted under light microscopy.
  
  
  RESULTS
  At 7 days after reperfusion, recovery of motor function was seen at varying degrees in groups B and C, whereas all animals in group A continued to exhibit paraplegia. In group C, most of the animals recovered to the baseline level, before creation of the ischemia model. A significant difference in numbers of viable neurons was found in group A (cell count, 10.1 +/- 4.7) and group C (cell count, 22.2 +/- 8.0) (p < 0.05). Higher numbers of viable motor neurons corresponded to a greater recovery of motor function.
  
  
  CONCLUSIONS
  These results suggest that cyclosporin A administration is effective against neuronal damage caused by spinal cord ischemia.
authors.affiliation: Department of Anesthesiology, Tohoku University Graduate School of Medicine, Sendai, Japan.
authors.forename: Minato
authors.initials: M
authors.lastname: Sato
authors.forename: Takashi
authors.initials: T
authors.lastname: Horinouchi
authors.forename: Masahiro
authors.initials: M
authors.lastname: Sakurai
authors.forename: Noritaka
authors.initials: N
authors.lastname: Murakami
authors.forename: Shun
authors.initials: S
authors.lastname: Sato
authors.forename: Masato
authors.initials: M
authors.lastname: Kato
mesh_terms: D000818:Animals; D016923:Cell Death / Q000187:drug effects; D016572:Cyclosporine / Q000494:pharmacology*; D004195:Disease Models, Animal; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D009046:Motor Neurons / Q000187:drug effects* / Q000473:pathology; D010264:Paraplegia / Q000517:prevention & control; D011817:Rabbits; D011897:Random Allocation; D020760:Spinal Cord Ischemia / Q000473:pathology*
chemical_list: D007166:Immunosuppressive Agents; D016572:Cyclosporine