The Role Of Optic Nerve Decompression In Optic Nerve Injury And Repair, And Clinical Effect,

Background and Objective The optic nerve injury is usually complicated with closed craniomaxillofacial trauma and direct trauma, and results in hypopsia and permanent visual loss. Optic nerve is a center nerve with characteristic of peripheral nerve. In traditional opinions, the capacity for CNS regeneration is much limited in adult mammals. Recently, following the advances in CNS regeneration, the topic on mechanism of optic nerve injury and regeneration has become an area of popular research. Optic nerve decompression was described by Kronlein in 1911. Since then, various approaches to optic nerve decompression were extensively utilized in clinical. The mechanisms of optic nerve injury and regeneration are still unclear at present, and there are no standard diagnoses and treatments of optic nerve injury. Optic nerve decompression is controversial in treatment of optic nerve injury. Optic nerve injury impairs the balance of constancy and plasticity of neuron. The damages cause a series of changes in electrophysiology, morphology and molecule neurobiology, such as the changing of expression of structural protein .In addition, in the local microenvironment around injured optic nerve various active compounds related to regeneration are produced which can regulate the extension of neurite. Growth Associated Protein increases obviously when nerve injured or regenerates, which can be regarded as an objective inner index to measure regeneration after nerve injury. Nitrogenmonoxide (NO) possesses bifunction to organism. Nitrogen monoxide synthase (NOS) is a rate-limiting enzyme to synthesis NO. The determination of NOS can reflect the role of NO in optic nerve injury. The purpose of thestudy was listed as follows.1. To investigate the regularity and functional mechanisms of theexpression of GAP-43 mRNA and iNOS mRNA following partial optic nerve injury in the course of injury and recovery. To provide reference for the study of the mechanisms of the optic nerve decompression in thenerve regeneration.2. To study the regularity and functional mechaisms of the expression of GAP-43 mRNA and iNOS mRNA following decompression of optic nerve after partial optic nerve injury. To study the molecular mechanism of action of the optic nerve decompression in the nerve recovery.Methods1. Adult New Zealand rabbits were used to create animal models of unilateral partial optic nerve injury under the condition of the same injury intensity. 30 New Zealand rabbits were separated randomly into six groups according to the expected postoperative survival periods: 1 day post injury(ldpi), 3 days post injury(3dpi), 7 days post injury(7dpi), 14 days post injury( 14dpi), 28 days post injury(28dpi), and 42 days post injury(42dpi). The right eye was the injured eye contrast to the left unharmed eye. The animals were sacrificed at the expected survival time.2. New Zealand rabbits were used to create animal models of hibateral partial optic nerve injury with the same injury intensity. 20 New Zealand rabbits were separated randomly into four groups according to the expected time for decompression: to decompress 1 day post injury(ldpi), 7 days post injury(7dpi), and 14 days post injury(Hdpi),. The right eye was the decompressive eye contrast to the left impaired eye. The animals were sacrificed four weeks after injury.3. By the expected survival time, flash visual evoked potential (F-VEP) wasdetected in both eyes of the model. Then, the animals were sacrificed and the eyes and optic nerve were enucleated. The expressions of GAP-43 mRNA and iNOS mRNA in distal part of optic nerve and lateral half of retina were explored by reverse transcriptive polymerase chain reaction (RT-PCR). Nicotinamide adenine dinucleotie phosphate (NADPH) was used as intra-reference. The proximal part of optic nerve and medialis half of retina were used for paraffin section. The average optical density (OD) of neural myelin sheath was stained by KB and the number of glial cells were detected and analyzed by the image analytical system of ImageJl .32j. All data were analyzed statistically by ANOVA or t test with the statistical software of SPSS 11.5 for windows. Results1. The morphologic changes showed: The optic nerve was demyelinated after injury. A peak was detected at 4 weeks after optic nerve injury. The proliferation of glial cells existed after injury and became obvious in the 4th and 6th weeks after injury.2. The optic nerves of all decompressive groups appeared demyelinated in the 4th week after injury. Optic nerve in the group of decompression 1dpi appeared less demyelinated after injury compared with controlled group and decompression 14 dpi group. The proliferation of glial cells after optic nerve injury lessened in all decompressive groups, but there was no significant difference compared with control group of injury.3. The results of visual evoked potential (VEP): the incubation period of P wave was lengthened, and the amplitude of wave was decreased. The outcome aggravated with the time.4. The incubation period and the amplitude of P wave of decompressive group 1dpi had no significant difference compared with the normal control groups, but had significant difference compared with injured groups. The other decompressive groups were reverse.5. The expression of GAP-43 mRNA gradually increased after OP1. There was no orless found to express in normal controlled groups. In the first day of postoperation, the distal tissues of injured retina and optic nerve started to express GAP-43 mRNA. The expressive intensity was stronger and stronger as the time went on. It peaked by the 4th week, and began to descent by the 6th week. There was no expression of iNOS mRNA in the normal group. While it started to express in the first day in the injured groups, and it peaked by the 7th day, down nearly to the normal by the 14th day.6. The expression of GAP-43 mRNA of retina in the group decompressed 1dpi was higher than in the injured group without decompression. The other groups had no significant difference compared with the injured groups . There was no expression of iNOS mRNA in all the decompressive groups.Conclusion1. Optic nerve injury can result in demyelination, neuroglia cell hyperplasia and the visual function impairment, which is concerned with the secondary lesion of optic nerve injury.2. The expression of GAP-43 mRNA in optic nerve and retina increases post optic nerve injury that is concerned with the spontaneous recovery of injured neurite.3. The expression of iNOS mRNA increases in retina after optic nerver injury which may concern with the secondary lesion of retina post optic nerve injury.4. The decompression of optic nerve in the earlier period after injury can lessen demyelination and improve vision function.5. The decompression of optic nerve in the earlier period after injury can elevate the expression of GAP-43 mRNA which may promote the process of neurite regeneration.