动物模型,外周性前庭损害 z-bo 2020-08-08 481

　　(1) Reproduction method Rats weighing about 200g and guinea pigs weighing about 500g have been checked to have clean external ear canal, complete tympanic membrane, no spontaneous nystagmus, and sharp hearing. ①The guinea pig was fixed under halothane inhalation anesthesia, and one side of the labyrinth was destroyed by chemical method. The skin of the temporal area was cut through aseptic operation and the tympanic vesicle wall was exposed. A small hole with a diameter of about 0.5mm was drilled with the tip of a scalpel. Inject 0.1 chloroform into the middle ear cavity through the hole, or through tympanic membrane puncture. ② Rats were anesthetized by intramuscular injection of a mixture of sodium pentobarbital (20 mg/kg body weight) and ketamine (60 mg/kg body weight), and then one side of the labyrinth was destroyed mechanically, and part of the alveolar bone wall was cut off with bone clamps; Cut the round window membrane aseptically under a microscope, expose the balloon, utricle, and ampullary ridge through the base of the cochlea. The plaque and ampullary ridge are silvery-white membranous material under the microscope; use a micro-aspirator to suck out the balloon and utricle Spot and ampullary crest, suture the wound. Closely observe the behavior of the model after operation. After all the experiments were completed, the rats and guinea pigs were anesthetized with pentobarbital sodium, the heart was exposed, the aorta was intubated through the left ventricular incision, and the solution was dissolved in warm normal saline containing 0.5% sodium nitrite. The animals were perfused with 10% formaldehyde solution in phosphate buffer, and the animals were sacrificed. The temporal bone specimens were taken out for pathological tissue sections, and the morphological changes of the vestibular structure were observed under the microscope.

　　(2) Model characteristics Guinea pigs have the first signs after injection of chloroform, that is, a group of unilateral vestibular dysfunction syndromes characterized by imbalance, the animals have horizontal nystagmus, and the slow phase is towards the injured side; The second symptom appeared after about 1 min. The animal rolled continuously along the long axis of the body on the medication side. After 1 min, it gradually slowed down and stopped rolling; the third symptom appeared immediately. The animal continued to crawl along the vertical axis of the ground on the medication side with its head. Tilt 20-30° to the medication side, staggering gait, shaking the body left and right, nystagmus, rolling, rotating. The incubation period of the second characteristic attack in rats is longer than that in guinea pigs. The post-mortem signs were nystagmus that lasted for nearly 1 week and long-term head tilt. After the labyrinth on one side of the injury, the background activity of the vestibular nerve on the injured side suddenly decreases, causing the tonic spontaneous discharge of the vestibular nucleus neurons to appear severely asymmetry on both sides, resulting in a significant increase in the efferent impulse of the vestibular motor reflex on one side, which induces Three major signs of nystagmus and imbalance between posture and movement. Histopathological observation under the microscope showed that the middle ear tissues all showed normal tissue morphology, and no pathological damage was found.

　　(3) Compared with previous medical research reports, animal models of peripheral vestibular damage can also be caused by total labyrinthectomy or vestibular neurotomy, but these models have limitations in studying vestibular compensation and decompensation mechanisms, and The surgical approach is relatively complicated and traumatic. The model replicated by this method avoids the above shortcomings, the surgical method is relatively simple, and the trauma is small. In order to explore the mechanism of compensation and decompensation for unilateral peripheral vestibular damage in clinic, clarify the clinical drug factors that may induce decompensation syndrome for patients in the compensated period, find new ways to treat peripheral vertigo, and improve clinical efficacy. The research provides an ideal animal model.