动物造模,标定性视神经损伤模型 z-bio 2021-03-29 689

　　(1) Breeding method Rats weighing 250-300 g confirmed by slit lamp microscope have double pupils of the same size and round shape, respond to light, and have obvious eye diseases and curved necks of adult rats, none. For anesthesia, a 3% sodium pentobarbital solution was injected intraperitoneally at a dose of 1 ml/kg body weight. The rat was fixed with a binocular operating microscope, perpendicular to the edge of the eyelid and cut into the upper orbital edge to cut the central part of the upper eyelid, and cut the bulbar conjunctiva and part of the conjunctiva in the same direction to expose the upper eyelid. The rectus muscles, separate the muscles. Completely separate the fascia along the superior rectus muscle to expose the optic nerve, cut the superior rectus muscle, clamp the broken end of the superior rectus muscle with fine-toothed forceps, and then pull the eyeball down completely. Expose the optic nerve. Using a special clamp with a clamping force of 40g to 2mm behind the ball, clamp the eyeball perpendicular to the optic nerve above the optic nerve for 4 seconds. At this time, the pupils gradually expand. Suture the conjunctiva and eyelid to layer.

　　(2) Model characteristics On the 4th day after optic nerve injury in rats, the recognition rate of retinal ganglion cells (RGC) was 77.79%, which was 22.21% lower than that of the normal control group, indicating that the optic nerve was directly clamped. Part of the axon transport is blocked. The RGC directly connected to the damaged nerve fiber loses its nutrient supply and causes irreversible death because the ganglion or external genital body nutrition cannot be transmitted to the RGC through the damaged nerve fiber.

　　(3) Comparative medicine The cause of blindness in glaucoma is the death of RGC due to optic nerve damage. High intraocular pressure is the main risk factor for optic nerve damage, but when about one-third of the patient's intraocular pressure is in the normal range, the visual field will continue to deteriorate. Therefore, it is speculated whether there are secondary risk factors for glaucomatous optic neuropathy. Optic nerve, such as acute and chronic ocular hypertension models, intravitreal injection of excitatory amino acid models, ischemia/reperfusion or hypoxia, to study the reasons for the continuous deterioration of the visual field of glaucoma patients after IOP control. The neural model has been established. Mechanical injury models, such as injury models that cause local death of the optic nerve or RGC, use retrograde or anterograde markers in quantitative and qualitative studies of RGCS to study persistent causes. After eliminating the main factors, optic nerve damage in patients with glaucoma. The model method uses a small force optic nerve clamp with a clamping force of 40 g. The nerve clamp clamped the optic nerve of the model rat for 4 seconds. After 4-21 days, the RGC loss rate was between 22.21% and 45.34%. , Indicating that an experimental animal model of glaucomatous optic neuropathy has been established. I succeeded that there are some similarities between this model and human glaucoma. In this animal model and human glaucoma, after removing the main factors that damage the optic nerve, the optic nerve further degenerates. Apoptosis and increased glutamate levels in eye cells. Therefore, the junctional optic nerve compression model can be used to study the etiology of glaucoma.