Objective： To introduce a new animal model of graded mechanical primary brainstem injury （BSI）. Methods： Altogether 45 rabbits were subjected to BSI by type II biological impact machine designed by the Third Mili...Objective： To introduce a new animal model of graded mechanical primary brainstem injury （BSI）. Methods： Altogether 45 rabbits were subjected to BSI by type II biological impact machine designed by the Third Military Medical University. The animals were divided into 4 experimental groups （n=10） and 1 control group （n=5） ac- cording to different magnitudes of impact pressure imposed on the occipital nodule： Group 1,500-520 kPa; Group 2, 520- 540 kPa; Group 3,540-560 kPa; Group 4, 560-580 kPa and Group 5, 0 kPa with 20 kPa increase in each grade. The im- pact depth was a constant 0.5 cm. After injury, the clinical symptoms and signs as well as pathological changes were observed. Results： Rabbits in Group 1 revealed mild physiologi- cal reaction of BSI. They had localized cerebral contusion with punctate hemorrhage and subarachnoid hemorrhage （SAH） was limited to the peripheral tissues at the impact area. In Group 2, obvious physiological reaction was observed. Local pathological lesions reached the superfi- cial layer of brainstem tissues; focal hemorrhage and girdle- shaped SAH in basilar pon were observed under microscope. In Group 3, BSI was more severe with a long respiratory depression. Pathological lesions reached the inner portionof brainstem with massive hemorrhage and the whole brainstem was wrapped by subarachnoid hematoma. In Group 4, most rabbits died due to severe BSI. Pathological lesions deepened to the central brainstem with wide patho- logical change, rapture of the medulla oblongata central canal. Group 5 was the control group, with normal brainstem structure and no lesion observed. Conclusion： This model successfully simulates differ- ent levels ofbrainstem mechanical injury and clearly shows the subsequent pathological changes following injury. It takes two external parameters （impact pressure and depth） and has a similar injury mechanism to clinical accelerating BSI. Moreover it is reproducible and stable, thus being be- neficial for exploring pathophysiological mechanism, diag- nosis and forensic identification of various degrees of BSI.展开更多
基金The paper was supported by the National Natural Science Foundation of China，the Natural Science Foundation of Chongqing of China，the Key Projects Foundation of the Ministry of Public Security
文摘Objective： To introduce a new animal model of graded mechanical primary brainstem injury （BSI）. Methods： Altogether 45 rabbits were subjected to BSI by type II biological impact machine designed by the Third Military Medical University. The animals were divided into 4 experimental groups （n=10） and 1 control group （n=5） ac- cording to different magnitudes of impact pressure imposed on the occipital nodule： Group 1,500-520 kPa; Group 2, 520- 540 kPa; Group 3,540-560 kPa; Group 4, 560-580 kPa and Group 5, 0 kPa with 20 kPa increase in each grade. The im- pact depth was a constant 0.5 cm. After injury, the clinical symptoms and signs as well as pathological changes were observed. Results： Rabbits in Group 1 revealed mild physiologi- cal reaction of BSI. They had localized cerebral contusion with punctate hemorrhage and subarachnoid hemorrhage （SAH） was limited to the peripheral tissues at the impact area. In Group 2, obvious physiological reaction was observed. Local pathological lesions reached the superfi- cial layer of brainstem tissues; focal hemorrhage and girdle- shaped SAH in basilar pon were observed under microscope. In Group 3, BSI was more severe with a long respiratory depression. Pathological lesions reached the inner portionof brainstem with massive hemorrhage and the whole brainstem was wrapped by subarachnoid hematoma. In Group 4, most rabbits died due to severe BSI. Pathological lesions deepened to the central brainstem with wide patho- logical change, rapture of the medulla oblongata central canal. Group 5 was the control group, with normal brainstem structure and no lesion observed. Conclusion： This model successfully simulates differ- ent levels ofbrainstem mechanical injury and clearly shows the subsequent pathological changes following injury. It takes two external parameters （impact pressure and depth） and has a similar injury mechanism to clinical accelerating BSI. Moreover it is reproducible and stable, thus being be- neficial for exploring pathophysiological mechanism, diag- nosis and forensic identification of various degrees of BSI.
