Experimental Studies. Depending On The Injection For The Treatment Of Traumatic Optic Atrophy And Its Mechanism

Objective: To establish an experimental animal mode! of opiic atrophy and then to determine the method of establishing this model. And then to investigate the effect and mechanism of Shiming Injection (a kind of preparation of Chinese medicine) on traumatic optic atrophy .Methods: In the first experiment , with a fixed amount of wound the rabbit model of traumatic optic atrophy(TOA) was established by reformative Klolein operation . after 20 and 40 days, all the studied rabbits were given the examinations of flash visual evoke response(F-VER) and pathomorphology . In the second experiment, 40 days after establishing TOA model by the same method , we given the TOA rabbits treatment with Shiming Injection for 30 days continuously . Then, we studied the effect of Shiming Injection on the visual function, axonal transport, pathologic changes, expression of some molecules and microcirculation of optic nerve by the examinations of F-VER, pathomorphology in light and electric scopes and immuncytochemisty.Results: In the visual function of optic nerve, F-VER was significantly lowered and the amount of optic nerve fiber was significantly decreased with a result of demyelination and neuroglia cell hyperplasia 40 days after establishing the TOA model. Shiming Injection improved F-VER, increased the amount of optic nerve fiber, alleviated pathological demyelination and inhibited hyperplasia of neurogiia cell. At the same time Shiming Injection accelerate the transportation of HorserAdish peroxidase (HRP) in axonal plasm and restrained the expression of ICAM-1. Additionally, Shiming Injection increased the expression of NT-3, CD34 and the content of neurofilament protein in optic nerve after treating with Shiming Injection for 30 days.Conclusion: About 40 days later, the experimental rabbit TOA model was established successfully by ligaturing optic nerve. Shiming Injection can treat experimental TOA efficiently by accelerating transportation of axonal plasm, improving the microenvironment and the microcirculation for optic nerve fiber to survive or regenerate and maintaining or rebuilding the microstructure of optic nerve fiber.