| Traumatic optic neuropathy is a common blinding clinical disease, because of its damage mechanism has not yet fully understood, the diagnosis and treatment has been the clinical difficulty. Based on the semi-quantitative damage of optic nerve, the establishment of the optic nerve crush animal model, simulating clinical optic nerve injury, dynamic observation after optic nerve crush manganese-enhanced magnetic resonance(MEMRI) optic nerve tracer imaging and pathology change, explore manganese-enhanced magnetic resonance imaging in the clinical application of the optic nerve injury:Observe the histomorphology changes after optic nerve contusion, and explore the change as the axon of nerve injury, for provide theoretical basis for the diagnosis and treatment after nerve injury.Methods:30healthy female SD rats, MEMRI and light microscopy were randomly divided into injury in1,2,5,90d groups, electron microscope examination were randomly divided into1,2d groups,3rats in each group, with its left eye as the experimental eye, right eye was control eye.Open temporal bulbar conjunctiva, the optic nerve was exposed, reverse50g force clamp after the ball2mm vertical optic nerve axis clamping10s, establishment of optic nerve crush model. Observe the morphological changes of optic nerve crush by light microscopy, electron microscopy.Each time before the group24h rats after intravitreal injection of concentration of Mncl2solution2μl30mmol/L. then for manganese enhanced magnetic resonance imaging tracking of optic nerve.Results:Optic nerve injury under light microscope mainly vacuolar degeneration of different degree of nerve fiber. Under electron microscope.1D axons dissolved, myelin loose solution, a gap is formed, the swelling of mitochondria. Group2D axons dissolved micro filament, microtubule aggravating, dissolved, massive vacuolization. mitochondrial swelling, vacuolation.Optic nerve crush in rats after intravitreal injection of Mncl2solution24h MRI examination, all T1WI control eye optic nerve showed, showed high signal display visual system, optic nerve, superior colliculus, the lateral genicμlate body part.1D group of experimental eyes crush site near eye end T1WI showed high signal, away from the eye end, signal is reduced;2D group of experimental eyes crush site near eye end T1WI showed high signal, away from the eye off the unseen;5D group and90d group on the T1WI experimental eye ball were unseen.Conclusion:1, The rat optic nerve crush model similar with human traumatic optic neuropathy, simple operation;2,Apparent pathological injury of nerve pathological changes with time and gradually increase;3,Optic axoplasmic transport function of manganese ion after optic nerve injury was significantly impaired, and increase with time, irreversible;4,Manganese-enhanced magnetic resonance can be observed in vivo optic nerve axoplasmic transport,can be explored the application in clinical. |
