title: Acute normovolemic hemodilution can aggravate neurological injury after spinal cord ischemia in rats.
abstract: BACKGROUND
  Acute normovolemic hemodilution (ANH) is currently performed during thoracoabdominal aortic surgery. However, the effects of ANH on spinal cord ischemic injury are currently unknown. Because hemodilution below a certain level of hematocrit (Hct) aggravates the neurological damage after cerebral ischemia, we hypothesized that ANH may increase neurological damage after spinal cord ischemia. The aim of these experiments was to determine the effects of ANH on spinal cord ischemic injury.
  
  
  METHODS
  Thirty male Sprague-Dawley rats were randomly assigned to 1 of the following 3 groups: no hemodilution (group C), target Hct level of 30% (group HD30), and target Hct level of 25% (group HD25). ANH was performed upon withdrawal of blood and simultaneous replacement with the same volume with hydroxyethyl starch. Spinal cord ischemia and reperfusion were induced by using a balloon-tipped catheter placed in the descending thoracic aorta, and changes in mean arterial blood pressure were recorded. Neurological function of the hindlimbs was evaluated for 7 days and recorded using a motor deficit score (MDS) (0 = normal; 5 = complete paraplegia). The number of motor neurons within the spinal cord was counted after final MDS evaluation.
  
  
  RESULTS
  Group HD25 developed hypotension during the latter part of the ANH procedure. Group C and group HD30 experienced 3 minutes of reperfusion hypotension, whereas 6 minutes of hypotension was observed in group HD25. Two rats in group HD25 died during the experimental period. Seven days after reperfusion, the MDS of group C, group HD30, and group HD25 was 1.0 (0.5-2.0), 1.0 (0.5-2.0), and 4.0 (2.8-4.2) (median [95% confidence interval]), respectively. Group HD25 showed significantly higher MDS compared with group C (corrected P = 0.0018; 95% CI for median difference = 1.0-3.5). Motor neuron numbers in the anterior horns of group C, group HD30, and group HD25 were 26.5 (25.0-27.5), 23.5 (22.0-26.5), and 12.5 (8.4-16.6) (median [95% CI]), respectively. Motor neuron numbers of group HD25 were significantly lower than those of group C (corrected P < 0.0001; 95% CI for median difference = 9.0-18.0).
  
  
  CONCLUSIONS
  The results of the present study indicate that intraoperative ANH to an Hct of 25%, combined with coincident hypotension, caused a delayed recovery of baseline mean arterial blood pressure during the reperfusion period and aggravated neurological outcome after spinal cord ischemia.
authors.affiliation: Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, Seongnamsi, Kyoneggido, Korea.
authors.forename: Jinhee
authors.initials: J
authors.lastname: Kim
authors.forename: Jinyoung
authors.initials: J
authors.lastname: Hwang
authors.forename: Jin
authors.initials: J
authors.lastname: Huh
authors.forename: Sahngun Francis
authors.initials: SF
authors.lastname: Nahm
authors.forename: Cheong
authors.initials: C
authors.lastname: Lim
authors.forename: Sanghyon
authors.initials: S
authors.lastname: Park
authors.forename: Sunghee
authors.initials: S
authors.lastname: Hahn
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D002404:Catheterization; D004195:Disease Models, Animal; D006400:Hematocrit; D006438:Hemodilution / Q000009:adverse effects*; D006895:Hydroxyethyl Starch Derivatives / Q000633:toxicity*; D007022:Hypotension / Q000209:etiology / Q000503:physiopathology; D008297:Male; D009043:Motor Activity; D009046:Motor Neurons / Q000473:pathology*; D010952:Plasma Substitutes / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020760:Spinal Cord Ischemia / Q000097:blood / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors
chemical_list: D006895:Hydroxyethyl Starch Derivatives; D010952:Plasma Substitutes