Deleterious versus neuroprotective effect of metabolic inhibition after traumatic spinal cord injury.
METHODS
This work is an experimental and prospective study in adult, female, Long-Evans rats.


OBJECTIVE
The aim of this study was to probe the effect of metabolic inhibition after an acute traumatic spinal cord injury (TSCI) using a standardized contusion model (NYU impactor) to know whether the metabolic inhibition is a 'secondary mechanism of injury' or a mechanism of protection.


METHODS
All experimental procedures were carried out in the Mexico City.


METHODS
Animals were divided into five groups: one sham and four with TSCI, including no treatment, rotenone (inhibitor of mitochondrial complex I), sodium azide (inhibitor of mitochondrial complex IV) and pyrophosphate of thiamine or non-degradable cocarboxylase as a metabolic reactivator.


RESULTS
After TSCI, the metabolic inhibition with sodium azide treatment diminished the lipid peroxidation process (malondialdehyde levels by spectrophotometric procedures) and the damage to the spinal cord tissue (morphometric analysis), and increased the activity of creatine kinase and lactate dehydrogenase enzymes (P<0.05) (measured by spectrophotometric procedures 24 h after TSCI as well as after the functional recovery of the hind limb (evaluated weekly for 2 months by the BBB (Basso, Beattie and Bresnahan) scale)) when compared with the TSCI group without treatment.


CONCLUSIONS
The results show that the partial and transitory inhibition of the aerobic metabolism after an acute TSCI could be a self-protection mechanism instead of being a 'secondary mechanism of injury'.
Torres
S
S
Research Medical Unit in Neurological Diseases, CMN, S XXI, IMSS, Mexico city, Mexico.
Salgado-Ceballos
H
H
Guizar-Sahagún
G
G
Torres
J L
JL
Orozco-Suarez
S
S
Diaz-Ruiz
A
A
Vázquez
M E
ME
Collado
C
C
Ríos
C
C
D000818:Animals; D003402:Creatine Kinase / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D045222:Electron Transport Chain Complex Proteins / Q000187:drug effects / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects* / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D007770:L-Lactate Dehydrogenase / Q000187:drug effects / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects / Q000502:physiology; D008297:Male; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D011446:Prospective Studies; D051381:Rats; D020318:Rats, Long-Evans; D020127:Recovery of Function / Q000187:drug effects / Q000502:physiology; D012402:Rotenone / Q000494:pharmacology; D019810:Sodium Azide / Q000494:pharmacology; D013116:Spinal Cord / Q000187:drug effects* / Q000378:metabolism* / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D013835:Thiamine Pyrophosphate / Q000494:pharmacology; D016896:Treatment Outcome; D014475:Uncoupling Agents / Q000494:pharmacology; D014803:Vitamin B Complex / Q000494:pharmacology
D045222:Electron Transport Chain Complex Proteins; D004791:Enzyme Inhibitors; D018696:Neuroprotective Agents; D014475:Uncoupling Agents; D012402:Rotenone; D014803:Vitamin B Complex; D019810:Sodium Azide; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D013835:Thiamine Pyrophosphate