The Models Of Open Craniocerebral Injury And Explosive Craniocerebral Injury At Simulated High Altitude In Rats

Objective: The models of open craniocerebral injury and explosive craniocerebral injury at simulated high altitude in rats were established and the characteristics of those craniocerebral injury models were investigated. Methods: (1) There were 200 rats in the open craniocerebral injury group and 210 rats in the explosive craniocerebral injury group. The animals were randomly divided into plain group and high altitude group. The open craniocerebral injury model in rats were established with a nailer gun shoot in rat head. The explosive craniocerebral injury model in rats were established with the explosion of detonator in an airtight metal chamber. Simulated high altitude conditions were established with a hypobaric chamber. (2) The brainstem auditory evoked potential after injury, brain water contents, Evans blue contents, and pathology in the two models at 1h, 6h, 12h, 24h, 48h, 72h and 168h after craniocerebral injury were regularly observed. (3) The regional cerebral blood flow (rCBF) and partial pressure of brain tissue oxygen (PbtO2) in the two models at the same time point above mentioned after craniocerebral injury were monitored respectively with Moor DRT4 laser doppler flowmetry and LICOX CMP instrument. Results: (1) The open craniocerebral injury and explosive craniocerebral injury models in rats were stable. (2) After the injury, there were some neurologic impairments and the higher death rates at the injury moment and at 1h after injury. The rates in high altitude group were higher than that in plain group. The incidence rate of apnea after explosive injury in high altitude group was higher than that in plain group. (3) The peak latencies and interpeak latencies of brainstem auditory evoked potential after injuries were significantly prolonged, and the value in high altitude group after injury were prolonged more significantly than that in plain group. (4) Brain water contents and Evans blue contents were increased immediately at 1h after injury, were maximized during 24-48h, began to restore at 72h , and couldn't return to the control level by 168h after injury.Brain water contents and Evans blue contents after injury in high altitude group were higher than those in plain group. (5)rCBF were decreased significantly at 1h after injury, were minimized during 48-72h afer injury, then began to restore , and couldn't return to thecontrol level by 168h after injury. The rCBF in high altitude group after injury were decreased more remarkably than that in plain group. (6) PbtO2 were decreased significantly at 1h after injury, were minimized during 24-48h after injury, then began to restore; The PbtO2 in high altitude group during 6-72h after injury were significantly lower than that in plain group. (7) The results of pathological change showed that , at the periphery of 3mm away from the lesion center, there were brain tissue ischemic changes during 1-6h after injury.The Nissl body decreased, mitochondrion swelling, slight increase of perivascular space, and edema of perivascular could be observed. By 24-48h, the changes above mentioned progressed, and from 72h after injury, began to restore. Compared with plain group , the pathologic changes in high altitude group were more obvious . (8) Light microscopy of Chinese ink-injected and image analysis showed , capillary density were decreased at 1h after injury, by 24-48h were minimized, and couldn't return to the control level by 168h after injury; the capillary density were more significantly reduced in high altitude group than that in plain group.Conclusions: (1) Using nailer gun shoot and the explosion of detonator in an airtight metal chamber and with a hypobaric chamber, the open craniocerebral injury and explosive craniocerebral injury models at simulated high altitude in rats can be establish successfully. (2) The results from our two models indicated that the brain edema were mainly vasogenic edema , exsited during early period after injury, and the brain edema progressed with time, began to restore at 72h after injury. After injury, t...