title: Does dexmedetomidine reduce secondary damage after spinal cord injury? An experimental study.
abstract: The aim of this experimental study was to investigate the possible protective effect of dexmedetomidine (DEX) on traumatic spinal cord injury (SCI). Twenty-two New Zealand rabbits were divided into three groups: sham (no drug or operation, n = 6), Control [SCI + single dose of 1 mL saline intraperitoneally (i.p), after trauma; n = 8] and DEX (SCI + 1 microg/kg dexmedetomidine in 1 mL, i.p, after trauma, n = 8). Laminectomy was performed at T10 and balloon angioplasty catheter was applied extradurally. Four and 24 h after surgery, rabbits were evaluated by an independent observer according to the Tarlov scoring system. Blood, cerebrospinal fluid (CSF), tissue samples from spinal cord were taken for biochemical and histopathological evaluations. After 4 h of SCI, all animals in control or DEX treated groups became paraparesic. On the other hand, 24 h after SCI, partial improvements were observed in both control and DEX treated groups. Traumatic SCI leads to increase in the lipid peroxidation and decreases enzymatic or nonenzymatic endogenous antioxidative defense systems. Again, SCI leads to apoptosis in spinal cord. DEX treatment slightly prevented lipid peroxidation and augmented endogenous antioxidative defense systems in CSF or spinal cord tissue, but failed to prevent apoptosis or neurodeficit after traumatic SCI. Therefore, it could be suggested that treatment with dexmedetomidine does not produce beneficial results in SCI.
authors.affiliation: Department of Neurosurgery, Faculty of Medicine, Afyon Kocatepe University, Ali Cetinkaya Kampusu, 03200, Afyon, Turkey. aaslan71@yahoo.com
authors.forename: Adem
authors.initials: A
authors.lastname: Aslan
authors.forename: Mustafa
authors.initials: M
authors.lastname: Cemek
authors.forename: Olcay
authors.initials: O
authors.lastname: Eser
authors.forename: Korhan
authors.initials: K
authors.lastname: Altunbaş
authors.forename: Mehmet Emin
authors.initials: ME
authors.lastname: Buyukokuroglu
authors.forename: Murat
authors.initials: M
authors.lastname: Cosar
authors.forename: Orhan
authors.initials: O
authors.lastname: Baş
authors.forename: Yuksel
authors.initials: Y
authors.lastname: Ela
authors.forename: Huseyin
authors.initials: H
authors.lastname: Fidan
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D020927:Dexmedetomidine / Q000494:pharmacology* / Q000627:therapeutic use; D004195:Disease Models, Animal; D018450:Disease Progression; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D005260:Female; D015227:Lipid Peroxidation / Q000187:drug effects / Q000502:physiology; D008297:Male; D009410:Nerve Degeneration / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D010264:Paraplegia / Q000188:drug therapy / Q000503:physiopathology / Q000517:prevention & control; D011817:Rabbits; D013116:Spinal Cord / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D017211:Treatment Failure
chemical_list: D000316:Adrenergic alpha-Agonists; D000975:Antioxidants; D018696:Neuroprotective Agents; D020927:Dexmedetomidine