Neurotrophic factors attenuate neuronal nitric oxide synthase upregulation, microvascular permeability disturbances, ede
Injury to the spinal cord is one of the important causes of disability in human population suffering from trauma and no success to treat this medical catastrophe has yet been achieved (Faden and Salzman, 1992; Faden, 1993). Paralysis, paraplegia and life-
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Chapter 8 Neurotrophic factors attenuate neuronal nitric oxide synthase upregulation, microvascular permeability disturbances, edema formation and cell injury in the spinal cord following trauma: an experimental study using topical application of BDNF and IGF-l in the rat H.
s. Sharma l , F. Nyberg2, T. Gordh 3, P. Alm4, and J. Westman! 1 Laboratory
of Neuroanatomy, Department of Medical Cell Biology, 2Department of Pharmaceutical Biosciences, Biomedical Centre, 3 Department of Anaesthesiology, University Hospital, Uppsala University, Uppsala, Sweden, and 4Department of Pathology, University Hospital, Lund University, Lund, Sweden
Introduction Injury to the spinal cord is one of the important causes of disability in human population suffering from trauma and no success to treat this medical catastrophe has yet been achieved (Faden and Salzman, 1992; Faden, 1993). Paralysis, paraplegia and life-time rehabilitation are the main problems of spinal cord injury victims throughout the world (Schwab and Bartholdi, 1996). Most of the incomplete spinal cord damage are at least partially reversible, if treated immediately following the primary insult. On the other hand, a delay in treatment schedule beyond 8 h following the primary insult, no significant neuroprotection is achieved irrespective of therapy (for review see Faden, 1993; Schwab and Bartholdi, 1996; Winkler et ai., 1998, for details see Chapters 14, 16, 17, 19 in this volume). Thus efforts should be made to treat trauma patients as soon as possible following initial traumatic events. Destructive changes in the spinal cord tissue occur within hours following trauma which is progressive with time leading to permanent disability (Sharma and Olsson, 1990; Olsson et ai., 1990; Sharma et ai., 1990a, Olsson et ai., 1995; Sharma et ai., 1995a; Schwab and Bartholdi, 1996). Pathophysiological studies of spinal cord and its reaction to cell injury in the past was characterised only following days or weeks after the initial insult (Schwab and Bartholdi, 1996). Thus, it is not certain whether
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these late pathological changes represent a reversible or irreversible damage to the cord. The early consequences of spinal trauma and its pathological reaction in relation with neuronal degeneration are not well known (Lipton, 1993; Faden and Salzman, 1992; Winkler et ai., 1998). A detailed knowledge of early cell reactions following trauma is necessary to explore suitable therapeutic measures to minimise cell and tissue injury (Sharma and Olsson, 1990; Sharma et ai., 1998c). A promising approach to reduce paraplegia or paralysis following spinal cord injury to enhance axonal regeneration has emerged recently (Schwab and Bartholdi, 1996). Regeneration and repair mechanisms may constitute one of the most important aspects of potential therapy in future for trauma victims. To enhance axonal regeneration use of neurotrophins, foetal tissue implants, or graft of peripheral nerves following trauma is suggested by several workers which is still preliminary and cu
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