How to make a nerve root animal model?

  The mechanical compression of nerve roots is not directly related to the occurrence of this disease. The inflammatory response of nerve roots, nutritional disorders, and conduction property damage are likely to be equally important.

  (1) Reproduction method Rats were anesthetized by intraperitoneal injection of sodium pentobarbital at a dose of 30 mg/kg body weight, and routinely prepared skin, disinfected, and draped, and marked the spinous process of the second thoracic vertebra. With neck 7 as the center, incise the skin and subcutaneous tissue along the spinous process longitudinally. The incision is about 1.5cm. Use a sharp knife to separate the muscles on both sides of the spinous process to expose the spinous process and the lamina on both sides. Use ophthalmic scissors to cut off the lamina above the transverse process on both sides of the neck 6, 7 to expose the spinal cord in the spinal canal. Use the nerve stripper to push the spinal cord to the right to expose the 6 and 7 nerve roots of the left neck. Place the quantitative filter paper soaked with formaldehyde under the axilla of the 6 and 7 nerve roots. Hemostasis carefully, sutured layer by layer, and aseptically bandaged.

  (2) Model characteristics 3 days after modeling, the nerve roots around the inflammatory substance in the model group were mainly severe vasodilatation, congestion, and nerve fiber edema, accompanied by a small amount of inflammatory cell response; 7 days after modeling, the model group The nerve roots around the inflammatory substances in rats are characterized by severe inflammatory cell infiltration. Accompanied by nerve fiber edema and degeneration; 14 days after the model was established, granulomas in the nerve roots around the inflammatory substance in the model group formed with a serious degree and multinucleated cells. Fibroblasts and collagen fibers still have varying degrees of inflammatory cell infiltration; 21 days after modeling, the collagen fibers in the nerve roots around the inflammatory material in the model group increased, and severe scarring developed.

  Rats appear to be inactive. If there are external factors, you can only crawl slowly with your right upper limb and both lower limbs. The left upper limb is close to your chest, not daring to touch the ground, elbow and wrist joints are not moving, and the second and third toes are tightened (it is estimated that it may be avoided Involving inflammatory and edema nerve roots, animal self-protective actions). At the same time, use a cotton swab to lightly touch the 7 nerve root distribution area of the neck, and the model mouse appears to dodge quickly. And continue to scream (it may be a phenomenon of hyperalgesia). Experimental observations show that the model mice's behaviors start to improve in about 2 weeks. The recovery of the movement is from the left upper limb not touching the ground, close to the chest, to the elbow joint touching the ground. Pain changes from hyperalgesia to less sensitive.

  The amplitude of somatosensory evoked potential N11 in model rats decreased, and the incubation period of N9~N13 was prolonged. At different postoperative periods, the content of substance P (a measure of pain sensitivity) in rat nerve roots increased significantly, and the content of PGE2 in rat plasma (reflecting severe inflammation Degree) has increased significantly.

  (3) Comparative medicine. The generation of radiculopathy of cervical spondylosis is essentially preceded by cervical spine degeneration. On the basis of nerve root canal stenosis, secondary physiological and biochemical changes of the injury appear metabolic disorders and metabolite stasis ( Such as highlighting the nucleus pulposus medium-like substance, acidic product accumulation), the release of biologically active substances (histamine, phospholipase A2, substance P, prostaglandin and other chemical substances) stimulation. Nerve roots are secondary to hyperemia, edema, inflammatory response and conduction damage. Among them, chemical radiculitis may be an important pathological and physiological factor of this disease. Through pathology, behavior, electrophysiology, and radioimmunoassay, it is fully demonstrated that the experimental method causes the inflammatory response of the rat cervical nerve root, which is in line with the pathological manifestations of radiculopathy in the acute phase.