Effects of antithrombin III on spinal cord-evoked potentials and functional recovery after spinal cord injury in rats.
METHODS
From the view of motor function, spinal cord-evoked potentials, and histology, we evaluated the effects of antithrombin III on a spinal cord injury resulting in incomplete paraplegia.


OBJECTIVE
To investigate the effect of antithrombin III on the recovery process after acute incomplete rat spinal cord injury.


BACKGROUND
Antithrombin III is used for treating disseminated intravascular coagulation by its anticoagulant effect and is also reported to reduce organ damage by the release of prostaglandin I2 from endothelial cells, induced by antithrombin III. Therefore, antithrombin III has potential as a therapeutic agent for spinal cord damage.


METHODS
The spinal cord injury was induced by placing a 25 g weight on the dorsal surface of the spinal cord at the 10th thoracic spine level for 20 minutes. Antithrombin III (250 U/kg) was administered intravenously 5 minutes before the compression, whereas 2 mL of physiologic saline solution was administered to the control group. We recorded the spinal cord-evoked potentials at the T13 level after stimulation of the brain and C7 level. For 12 weeks after the injury, we observed the recovery course of waveform and motor function. The recovery of motor function was evaluated by using inclined table and modified Tarlov scores. We also examined the histology of the compressed site in the spinal cord.


RESULTS
There were statistically significant differences in the motor recovery process between the two groups. Evoked potentials of the antithrombin III group recovered earlier than those of the control group. Histologically, hemorrhage and tissue defects in the spinal cord were less in the antithrombin III group.


CONCLUSIONS
Because antithrombin III facilitated the recovery of behavior and evoked potentials, these findings suggest that antithrombin III may have a positive effect on the recovery of incomplete spinal cord injury.
Arai
Makoto
M
Department of Orthopedic Surgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan. mkt.arai-k@komagome-hospital.bunkyo.tokyo.jp
Goto
Takahiro
T
Seichi
Atsushi
A
Nakamura
Kozo
K
D000818:Animals; D000990:Antithrombin III / Q000627:therapeutic use*; D001921:Brain / Q000502:physiology; D004195:Disease Models, Animal; D004558:Electric Stimulation / Q000379:methods; D005071:Evoked Potentials / Q000187:drug effects*; D006614:Hindlimb / Q000503:physiopathology; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D010264:Paraplegia / Q000209:etiology / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000187:drug effects; D020127:Recovery of Function / Q000187:drug effects*; D013116:Spinal Cord / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D013117:Spinal Cord Compression / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D016896:Treatment Outcome
D000990:Antithrombin III