Neurosurgical Review

, Volume 21, Issue 2–3, pp 117–120 | Cite as

The effect of duration of compression on lipid peroxidation after experimental spinal cord injury

  • Mehmet Yaşar Kaynar
  • Murat Hanci
  • Ali Kafadar
  • Koray Gümüştaş
  • Ahmed Belce
  • Nejat Çiplak


The present study was performed to evaluate the effect of duration of acute spinal cord compression on tissue lipid peroxidation in rats. A clip compression method (1) was used to produce acute spinal cord injury. Rats were divided into 3 groups, each consisting of 10. At 1 hour after trauma all rats were sacrificed, and MDA content of the injured spinal cord segment was measured. The tissue MDA contents were 3.922 μmolMDA/gww in group 1 (control), 10.192 μmol MDA/gww in group 2 (30 seconds compression), and 12.147 μmolMDA/gww in group 3 (60 seconds compression). These results demonstrate that the length of duration of compression significantly enhances lipid peroxidation. Our study supported the view that persisting compression may cause progression of secondary mechanisms which may irreversibly eliminate any potential for recovery.


Experimental spinal cord injury lipid peroxidation 


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  1. [1]
    Anderson DK, P Demediuk, RD Saunders et al: Spinal cord injury and protection. Ann Emerg Med 14 (1985) 816–821CrossRefPubMedGoogle Scholar
  2. [2]
    Anderson DK, RD Saunders, P Demediuk et al: Lipid hydrolysis and peroxidation in injured spinal cord: partial protection with methylprednisolone or vitamin E and selenium. Cent Nerv Syst Trauma 2 (1985) 257–267PubMedGoogle Scholar
  3. [3]
    Anderson DK, ED Means, TR Waters et al: Spinal cord energy metabolism following compression trauma to the feline spinal cord. J Neurosurg 53 (1980) 375–380PubMedGoogle Scholar
  4. [4]
    Anderson DK, LD Prockop, ED Means et al: Cerebrospinal fluid lactate and electrolyte levels following experimental spinal cord injury. J Neurosurg 44 (1976) 715–722PubMedGoogle Scholar
  5. [5]
    Anderson DK, ED Hall: Pathophysiology of spinal cord trauma. Ann Emerg Med 22 (1993) 987–92CrossRefPubMedGoogle Scholar
  6. [6]
    Balentine JD, CW Hilton: Ultrastructural pathology of axons and myelin in calciuminduced myelopathy. Journal of Neuropathology and Experimental Neurology 39 (1980) 339Google Scholar
  7. [7]
    Balentine JD, CW Hilton: Calcifications of axons in experimental spinal cord trauma. Annals of Neurology 2 (1980) 520–523Google Scholar
  8. [8]
    Banik NL, EL Hogan, CY Hsu: Molecular and anatomical correlates of spinal cord injury. CNS Trauma 2 (1985) 99–107Google Scholar
  9. [9]
    Barut S, A Canbolat, T Bilge, Y Aydin, B Çokneşeli, U Kaya: Lipid peroxidation in experimental spinal cord injury: time-level relationship. Neurosurg Rev 16 (1993) 53–59CrossRefPubMedGoogle Scholar
  10. [10]
    Bracken MB, MJ Shepard, WF Collins, TR Holford, W Young, DS Baskin et al: A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal cord injury: Results of the second NASCIS. N Engl J Med 322 (1990) 1405–11PubMedGoogle Scholar
  11. [11]
    Braughler JM, ED Hall: Lactate and pyruvate metabolism in injured cat spinal cord before and after a single large intravenous dose of methylprednisolone. J Neurosurg 59 (1983) 256–261PubMedGoogle Scholar
  12. [12]
    Casini AF, M Ferrali, A Pampella, E Maellaro, M Comporti: Lipid peroxidation and cellular damage in extrahepatic tissues of Bromobenzene-intoxicated mice. Am J Pathol 123 (1986) 520–531PubMedGoogle Scholar
  13. [13]
    Clendenon NR, N Allen, WA Gordon et al: Inhibition of Na+-K+-activated ATPase activity following experimental spinal cord trauma. J Neurosurg 49 (1978) 563–568PubMedGoogle Scholar
  14. [14]
    Demediuk P, RD Saunders, DK Anderson et al: Membrane lipid changes in laminectomized and traumatized cat spinal cord. Proc Nat Acad Sci USA 82 (1985) 7071–7075PubMedGoogle Scholar
  15. [15]
    Demopoulos HB, ES Flamm, ML Seligman et al: Further studies on free-radical pathology in the major central nervous system disorders: effect of very high doses of methylprednisolone on the functional out-come, morphology and chemistry of experimental spinal cord impact injury. Can J Physiol Pharmacol 60 (1982) 1415–1424PubMedGoogle Scholar
  16. [16]
    Dolan EJ, CH Tator, L Endrenyi: The value of decompression for acute experimental spinal cord compression injury. J Neurosurg 53 (1980) 749–755PubMedGoogle Scholar
  17. [17]
    Guha A, CH Tator, L Endrenyi, I Piper: Decompression of the spinal cord improves reovery after acute experimental spinal cord compression injury. Paraplegia 25 (1987) 324–339PubMedGoogle Scholar
  18. [18]
    Hall ED: Lipid antioxidants in acute central nervous system injury. Ann Emerg Med 22 (1993) 1022–7PubMedGoogle Scholar
  19. [19]
    Hall ED: Neuroprotective actions of glucocorticoid and nonglucocorticoid steroids in acute neuronal injury. Cell Mol Neurobiol 13 (1993) 415–32CrossRefPubMedGoogle Scholar
  20. [20]
    Hall ED, JM Braughler: Effects of intravenous methylprednisolone on spinal cord lipid peroxidation and Na+-K+ ATPase activity. Dose response analysis during first hour after contusion injury in the cat. J Neurosurg 57 (1982) 247–253PubMedGoogle Scholar
  21. [21]
    Hall ED, JM Braughler: Free radicals in CNS injury. Res Publ Assoc Res Nerv Ment Dis 71 (1993) 81–105PubMedGoogle Scholar
  22. [22]
    Hall ED, RJ Traystman: Secondary tissue damage after CNS injury. Current concepts. The Upjohn Company, Kalamazoo, Michigan (1993)Google Scholar
  23. [23]
    Happel ED, KP Smith, MC Banik, JM Powers, EL Hogan, JD Balentine: Ca++ accumulation in experimental spinal cord trauma. Brain Research 211 (1981) 476–479CrossRefPubMedGoogle Scholar
  24. [24]
    Hsu CY, PV Halusha, EL Hogan et al: Alteration of thromboxane and prostacyclin levels in experimental spinal cord injury. Neurology 35 (1985) 1003–1009PubMedGoogle Scholar
  25. [25]
    Ildan F, S Polat, A Öner, T Isbir, AL Göçer, O Tap, M Kaya, A Karadayi: Effect of naloxone on sodium and potassium activated and magnesium dependent ATPase activity and lipid peroxidation and early ultrastructural findings after experimental spinal cord injury. Neurosurg 36 (1995) 797–805Google Scholar
  26. [26]
    Kurihara M: Role of monoamines in experimental spinal cord injury in rats. Relationship between Na+-K+-ATPase and lipid peroxidation. J Neurosurg 62 (1985) 743–749PubMedGoogle Scholar
  27. [27]
    Rivlin AS, CH Tator: Effect of duration of acute spinal cord compression in a new acute cord injury model in the rat. Surg Neurol 10 (1978) 39–43Google Scholar
  28. [28]
    Stokes BT, P Fox, G Hollinden: Extracellular calcium activity in the injured spinal cord. Experimental Neurology 80 (1983) 561–572CrossRefPubMedGoogle Scholar
  29. [29]
    Tarlov IM: Spinal cord compression studies III. Time limits for recovery after gradual compression in dogs. Arch Neurol Psychiatry 71 (1954) 588–597Google Scholar
  30. [30]
    Tarlov IM, H Klinger: Spinal cord compression studies II. Time limits for recovery after acute compression in dogs. Arch Neurol Psychiatry 71 (1954) 271–290Google Scholar
  31. [31]
    Wheeler KP, JA Walker, DM Barker: Lipid requirement of the membrane sodium plus potassium iondependent ATPase system. Biochem J 146 (1975) 713–722PubMedGoogle Scholar
  32. [32]
    Wolfe LS: Eicosanoids: prostaglandin, thromboxanes, leukotrienes and other derivatives of carbon-20 unsaturated fatty acids. Journal of Neurochemistry 38 (1982) 1–14PubMedGoogle Scholar

Copyright information

© Walter de Gruyter GmbH & Co 1998

Authors and Affiliations

  • Mehmet Yaşar Kaynar
    • 1
  • Murat Hanci
    • 1
  • Ali Kafadar
    • 1
  • Koray Gümüştaş
    • 2
  • Ahmed Belce
    • 2
  • Nejat Çiplak
    • 1
  1. 1.Department of NeurosurgeryIstanbul University Cerrahpaşa Medical FacultyAksaray IstanbulTurkey
  2. 2.Department of BiochemistryIstanbul University Cerrahpaşa Medical FacultyAksaray IstanbulTurkey

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