Systemic hypothermia following spinal cord compression injury in the rat: axonal changes studied by beta-APP, ubiquitin, and PGP 9.5 immunohistochemistry.
METHODS
Systemic hypothermia exerts neuroprotective effects in experimental ischemic CNS models caused by vascular occlusions. Recent experimental and clinical studies have also demonstrated beneficial effects of hypothermic treatment following brain trauma.


OBJECTIVE
The present study addresses the question as to whether systemic hypothermia has similar protective qualities following severe spinal cord compression trauma using beta-APP-, ubiquitin-, and PGP-9.5-immunohistochemistry combined with the ABC complex method as markers to identify axonal changes.


METHODS
Fifteen rats were randomized into three equally large groups and sustained to either thoracic laminectomy or to severe spinal cord compression trauma of the Th 8 - 9 segments. The non-trauma group contained laminectomized animals submitted to a hypothermic procedure in which the core temperature was reduced from 38 to 30 degrees C. The two trauma groups were either submitted to the same hypothermic procedure or kept normothermic during the corresponding time. All animals were sacrificed 24 h following the surgical procedure.


RESULTS
In the hypothermic non-trauma group no axonal changes were seen. The number of abnormal axons, as indicated by accumulation of immunoreactive material in enlarged axons, was lower in the peri-injury zones of the hypothermic trauma group than in the normothermic trauma group. This difference was most obvious in the cranial peri-injury zones. No differences were seen between the groups in the trauma zones.


CONCLUSIONS
This study demonstrates reduced axonal swelling in the peri-injury zones of spinal cord injured rats treated with systemic hypothermia. These changes could either indicate neuroprotective effects of the hypothermic treatment, or be results of reduced axonal transport or protein synthesis. To evaluate the clinical importance of our findings, further studies including reliable outcome measures of the animals must be performed.
Westergren
H
H
Section of Neurosurgery, Department of Neuroscience, Uppsala University, Sweden.
Yu
W R
WR
Farooque
M
M
Holtz
A
A
Olsson
Y
Y
D016564:Amyloid beta-Protein Precursor / Q000032:analysis*; D000818:Animals; D001369:Axons / Q000473:pathology*; D001831:Body Temperature / Q000502:physiology; D007036:Hypothermia, Induced; D007150:Immunohistochemistry; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000473:pathology*; D013117:Spinal Cord Compression / Q000473:pathology* / Q000503:physiopathology; D013869:Thiolester Hydrolases / Q000032:analysis*; D013997:Time Factors; D043222:Ubiquitin Thiolesterase; D014452:Ubiquitins / Q000032:analysis*
D016564:Amyloid beta-Protein Precursor; D014452:Ubiquitins; D013869:Thiolester Hydrolases; D043222:Ubiquitin Thiolesterase