title: Neuroprotection following mild hypothermia after spinal cord ischemia in rats.
abstract: OBJECTIVE
  We examined the hypothesis that a 1°C reduction in body temperature would reduce gray and white matter injury induced by spinal cord ischemia in rats. In addition, we evaluated the relationship between reactive astrogliosis and gray or white matter injury after spinal cord ischemia with a 1°C reduction in body temperature or normothermia.
  
  
  METHODS
  Rats were randomly divided into hypothermia (1°C decrease in body temperature to 36.3°C), normothermia (37.3°C), and sham surgery groups (n=6/group). Hypothermia was induced 15 minutes before ischemia and maintained during ischemia. Animals were then rewarmed to normothermia. Spinal cord ischemia was induced by a balloon catheter in the thoracic aorta, and the proximal mean arterial blood pressure was maintained at 40 mm Hg for 14 minutes. Hind limb motor function was assessed at 2, 7, 14, 21, and 28 days after reperfusion. At 28 days after reperfusion, gray matter damage was assessed by counting the number of normal motor neurons and white matter damage by the extent of vacuolation. The glial fibrillary acidic protein (GFAP)-positive area fraction (GFAP%) was determined in white and gray matter structures to measure reactive astrogliosis.
  
  
  RESULTS
  Compared with normothermia, hypothermia significantly improved hind limb function at all assessments (P<.01) and increased numbers of normal gray matter motor neurons (39±20 vs 99±13, respectively; P<.001), decreased the percentage area of white matter vacuolation (9.0%±2.7% vs 1.6%±1.3%, respectively; P=.001), and decreased the GFAP% in gray (P=.003) and white matter (P=.009).
  
  
  CONCLUSIONS
  Prophylactic mild hypothermia (1°C reduction in body temperature) preserved hind limb motor function and reduced neuronal death, white matter vacuolation, and astrogliosis in gray and white matter induced by spinal cord ischemia in rats. Thus, mild hypothermia may be useful for perioperative management of thoracoabdominal aortic surgery.
authors.affiliation: Division of Thoracic and Cardiovascular Surgery, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. saito@med.niigata-u.ac.jp
authors.forename: Takeshi
authors.initials: T
authors.lastname: Saito
authors.forename: Shino
authors.initials: S
authors.lastname: Saito
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yamamoto
authors.forename: Masanori
authors.initials: M
authors.lastname: Tsuchida
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000503:physiopathology; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D021721:Balloon Occlusion; D015415:Biomarkers / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D001930:Brain Injuries / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000209:etiology / Q000473:pathology / Q000517:prevention & control; D006614:Hindlimb; D007036:Hypothermia, Induced; D007150:Immunohistochemistry; D008297:Male; D009046:Motor Neurons / Q000473:pathology*; D018482:Muscle, Skeletal / Q000294:innervation*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D020760:Spinal Cord Ischemia / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D013997:Time Factors
chemical_list: D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein