Erdosteine ameliorates neurological outcome and oxidative stress due to ischemia/reperfusion injury in rabbit spinal cord.
OBJECTIVE
Oxygen-derived free radicals have been suggested as important in degeneration after spinal cord ischemia. The aim of this study was to investigate whether erdosteine has a protective effect against spinal cord ischemia during aortic cross clamping.


METHODS
New Zealand White rabbits (n=21) were divided into three groups. In the ischemia/reperfusion group (I/R) (n=8), the infrarenal aorta of rabbits was cross clamped for 21 min and then reperfused. In erdosteine group, the administration of erdosteine solution (50 mg/kg) was started two days before aortic cross-clamping and rabbits (n=8) were subjected to ischemia and reperfusion. Animals in control group (n=5) underwent a surgical procedure similar to the other groups but the aorta was not clamped. The animals were sacrificed at 72 h and histopathological, and biochemical analyses were carried out on the lumbar spinal cords.


RESULTS
Erdosteine treatment was associated with improved neurological function in the postoperative period. Histopathological examination of spinal cord tissues in erdosteine group revealed changes consistent with mild ischemic injury, but rabbits in I/R group with paraplegia had total destruction of the motor neurons. Biochemical analyses of spinal cord tissues, in the I/R group, revealed a significant increase in the superoxide dismutase, xanthine oxidase, adenosine deaminase and myeloperoxidase activities, and a significant depletion in glutathione peroxidase activity when compared to that of control rabbits. Erdosteine treatment prevented the increase of all these enzymes except adenosine deaminase. Ischemia/reperfusion produced a significant increase in the tissue malondialdehyde levels. Ischemia/reperfusion-induced increments in malondialdehyde content of the spinal cord were significantly prevented by erdosteine treatment.


CONCLUSIONS
The present study demonstrated that erdosteine treatment before aortic cross clamping ameliorates neurological outcome, neuronal injury and oxidative stress in the rabbit spinal cord.
Ege
E
E
Department of Cardiovascular Surgery, Turgut Ozal Medical Center, Inonu University, Malatya, Turkey.
Ilhan
A
A
Gurel
A
A
Akyol
O
O
Ozen
S
S
D000243:Adenosine Deaminase / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D001012:Aorta, Abdominal / Q000378:metabolism / Q000473:pathology; D015415:Biomarkers / Q000097:blood; D004195:Disease Models, Animal; D005100:Expectorants / Q000627:therapeutic use*; D005979:Glutathione Peroxidase / Q000187:drug effects / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D008955:Models, Cardiovascular; D009046:Motor Neurons / Q000187:drug effects / Q000473:pathology; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D011597:Psychomotor Performance / Q000187:drug effects; D011817:Rabbits; D015427:Reperfusion Injury / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology*; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology*; D020760:Spinal Cord Ischemia / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000187:drug effects / Q000378:metabolism; D013864:Thioglycolates / Q000627:therapeutic use*; D013876:Thiophenes / Q000627:therapeutic use*; D016896:Treatment Outcome; D014969:Xanthine Oxidase / Q000187:drug effects / Q000378:metabolism
D015415:Biomarkers; D005100:Expectorants; D018696:Neuroprotective Agents; D013864:Thioglycolates; D013876:Thiophenes; D009569:Nitric Oxide; D008315:Malondialdehyde; C048498:erdosteine; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D014969:Xanthine Oxidase; D000243:Adenosine Deaminase