{"title":"大鼠外伤性脑损伤:中线流体冲击模型的表征。","authors":"T K McIntosh, L Noble, B Andrews, A I Faden","doi":"10.1089/cns.1987.4.119","DOIUrl":null,"url":null,"abstract":"<p><p>Fluid-percussion models of traumatic brain injury produce injury by rapidly injecting fluid volumes into the epidural space. In the present study, we characterized the physiological, histopathological, and neurological responses in a new model of midline (vertex) fluid-percussion injury of graded severity in the rat. All levels of injury produced transient (acute) hypertension, which was followed by a significant and prolonged hypotension at the higher levels of injury. There was also postinjury suppression if EEG amplitudes, which was related to the severity of injury. However, there were no significant changes in brainstem auditory evoked potentials (BAERs) at any level of injury. Neurological scores over a 4-week postinjury period were directly correlated with the severity of injury. Survival rates were significantly decreased at the higher magnitudes of injury. The extent of postinjury hemorrhage and blood-brain barrier disruption (as evidenced by extravasation of Evans Blue Albumin complex) was related to the magnitude of injury. These data demonstrate that the midline (vertex) model of fluid-percussion injury in the rat reproduces many of the features of head injury observed in other models and species and may serve as a useful cost-effective model for the study of the pathophysiology and treatment of traumatic brain injury.</p>","PeriodicalId":77690,"journal":{"name":"Central nervous system trauma : journal of the American Paralysis Association","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cns.1987.4.119","citationCount":"232","resultStr":"{\"title\":\"Traumatic brain injury in the rat: characterization of a midline fluid-percussion model.\",\"authors\":\"T K McIntosh, L Noble, B Andrews, A I Faden\",\"doi\":\"10.1089/cns.1987.4.119\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Fluid-percussion models of traumatic brain injury produce injury by rapidly injecting fluid volumes into the epidural space. In the present study, we characterized the physiological, histopathological, and neurological responses in a new model of midline (vertex) fluid-percussion injury of graded severity in the rat. All levels of injury produced transient (acute) hypertension, which was followed by a significant and prolonged hypotension at the higher levels of injury. There was also postinjury suppression if EEG amplitudes, which was related to the severity of injury. However, there were no significant changes in brainstem auditory evoked potentials (BAERs) at any level of injury. Neurological scores over a 4-week postinjury period were directly correlated with the severity of injury. Survival rates were significantly decreased at the higher magnitudes of injury. The extent of postinjury hemorrhage and blood-brain barrier disruption (as evidenced by extravasation of Evans Blue Albumin complex) was related to the magnitude of injury. These data demonstrate that the midline (vertex) model of fluid-percussion injury in the rat reproduces many of the features of head injury observed in other models and species and may serve as a useful cost-effective model for the study of the pathophysiology and treatment of traumatic brain injury.</p>\",\"PeriodicalId\":77690,\"journal\":{\"name\":\"Central nervous system trauma : journal of the American Paralysis Association\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1987-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1089/cns.1987.4.119\",\"citationCount\":\"232\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Central nervous system trauma : journal of the American Paralysis Association\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1089/cns.1987.4.119\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Central nervous system trauma : journal of the American Paralysis Association","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1089/cns.1987.4.119","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Traumatic brain injury in the rat: characterization of a midline fluid-percussion model.
Fluid-percussion models of traumatic brain injury produce injury by rapidly injecting fluid volumes into the epidural space. In the present study, we characterized the physiological, histopathological, and neurological responses in a new model of midline (vertex) fluid-percussion injury of graded severity in the rat. All levels of injury produced transient (acute) hypertension, which was followed by a significant and prolonged hypotension at the higher levels of injury. There was also postinjury suppression if EEG amplitudes, which was related to the severity of injury. However, there were no significant changes in brainstem auditory evoked potentials (BAERs) at any level of injury. Neurological scores over a 4-week postinjury period were directly correlated with the severity of injury. Survival rates were significantly decreased at the higher magnitudes of injury. The extent of postinjury hemorrhage and blood-brain barrier disruption (as evidenced by extravasation of Evans Blue Albumin complex) was related to the magnitude of injury. These data demonstrate that the midline (vertex) model of fluid-percussion injury in the rat reproduces many of the features of head injury observed in other models and species and may serve as a useful cost-effective model for the study of the pathophysiology and treatment of traumatic brain injury.