【Animal Modeling】-Rat Lumbar Spinal Canal Stenosis Model

  (1) Replication method Rats are anesthetized by intraperitoneal injection of phenobarbital at a dose of 50 mg/kg body weight. After anesthesia, the rat was fixed prone on the surgical board for lumbar spinal surgery. From the animal’s third lumbar vertebrae to the sacrum, a longitudinal incision was made. The paraspinal muscles on both sides were stripped and the fifth lumbar vertebral lamina and upper and lower joint protrusions were removed at the same time. The lower articular protrusion of the 4th lumbar vertebrae and the upper articular protrusion of the 6th lumbar vertebrae, take the right iliac bone, and transplant the excised lumbar lamina bone fragments to the epidural, and be careful not to damage the cauda equina. Animals are raised regularly and eat freely.

  (2) Model characteristics: 9 months after modeling, the response of model animals to thermal stimulation was lower than before. Electrophysiological measurements showed that SSEP of model animals was significantly lower than normal animals at 8 or 9 months after operation. The average cross-sectional area of the fifth lumbar spinal canal of model animals was reduced by nearly 50% compared with normal control animals. At the same time, the model animals have severe adhesion of nerve roots and obvious stenosis of the spinal canal. There are also obvious adhesions between cauda equina nerve fibers and adhesion to the dura; the nerve fibers are obviously degeneration, the thick fibers are obviously disappeared, and the swollen interstitium is scattered with fine fibers. The blood vessel wall in the nerve fiber is hypertrophy, the number of interstitial cells increases and it is obviously swollen.

  (3) Comparative medicine This model adopts extensive excision of the vertebral arch of the fifth lumbar vertebrae and bone transplantation to produce chronic progressive lumbar spinal stenosis, thereby establishing an animal model of lumbar spinal stenosis. Walking analysis showed that the bipedal angle and distance of the step type were significantly impaired, and the abnormal gait of bipedal jumping occurred at the end of walking. The walking distance was reduced by about 80% compared with the control group. The gait returned to the original gait after a few minutes of rest. These results are comparable to movement disorders and intermittent claudication caused by lumbar spinal stenosis. According to the response time to the thermal stimulus to evaluate the change of sensory function. Compared with normal control animals, this model has a shorter reaction time of more than 50% at 9 months after surgery, and the lower limbs of model rats have hypersensitivity. These changes are consistent with the chronic course of cauda equina compression. SSEP, as a means of evaluating cauda equina compression damage, has obvious significance both in clinical and experimental. In the animal model of cauda equina compression experiment, the sensitivity of cauda equina nerve is increased after compression. The cauda equina nerve of the model animal established by this method may have obvious conduction obstacles. The pathological tissue section of the fifth lumbar spinal canal was taken to understand the spinal canal stenosis and the degeneration of the cauda equina. The results of microscopic observation showed that there was no obvious stenosis of the spinal canal in the model animal 1 month after surgery, and no degeneration of the cauda equina nerve was seen. Adhesion, and the mean value of the cross-sectional area of the spinal canal of the model animal was significantly reduced at 9 months after the operation. The cauda equina nerve fibers were significantly degenerated, and a series of pathological changes that were very similar to clinically human lumbar spinal stenosis.