Morphological changes of the neural cells after blast injury of spinal cord and neuroprotective effects of sodium beta-aescinate in rabbits

Injury. 2010 Jul;41(7):707-16. doi: 10.1016/j.injury.2009.12.003. Epub 2010 Jan 12.

Abstract

Objective: Explosive blast neurotrauma is becoming more and more common not only in the military population but also in civilian life due to the ever-present threat of terrorism and accidents. However, little attention has been offered to the studies associated with blast wave-induced spinal cord injury in the literatures. The purpose of this study is to report a rabbit model of explosive blast injury to the spinal cord, to investigate the histological changes, focusing especially on apoptosis, and to reveal whether beta-aescinate (SA) has the neuroprotective effects against the blast injury.

Methods: Adult male New Zealand white rabbits were randomly divided into sham group, experimental group and SA group. All rabbits except the sham group were exposed to the detonation, produced by the blast tube containing 0.7 g cyclotrimethylene trinitramine, with the mean peak overpressure of 50.4 MP focused on the dorsal surface of T9-T10 level. After evaluation of the neurologic function, spinal cord of the rabbits was removed at 8 h, 1, 3, 7, 14 or 30 days and the H&E staining, EM examination, DNA gel electrophoresis and TUNEL were progressively performed.

Results: The study demonstrated the occurrence of both necrosis and apoptosis at the lesion site. Moreover, the SA therapy could not only improve the neurologic outcomes (P<0.05) but also reduce the loss of motoneuron and TUNEL-positive rate (P<0.05).

Conclusions: In the rabbit model of explosive blast injury to the spinal cord, the coexistent apoptotic and necrotic changes in cells was confirmed and the SA had neuroprotective effects to the blast injury of the spinal cord in rabbits. This is the first report in which the histological characteristics and drug treatment of the blast injury to the spinal cord is demonstrated.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Blast Injuries / complications
  • Blast Injuries / pathology*
  • Disease Models, Animal
  • Drug Evaluation, Preclinical / methods
  • Male
  • Neurons / drug effects
  • Neuroprotective Agents / therapeutic use*
  • Rabbits
  • Sodium Compounds / therapeutic use*
  • Spinal Cord / drug effects
  • Spinal Cord / pathology*
  • Spinal Cord Injuries / drug therapy
  • Spinal Cord Injuries / pathology*
  • Spinal Cord Ischemia / drug therapy
  • Spinal Cord Ischemia / pathology*

Substances

  • Neuroprotective Agents
  • Sodium Compounds