Please use this identifier to cite or link to this item:
|Title:||Only mass lesions increase intracranial pressure in rats after lateral fluid percussion brain injury and secondary hypoxia|
|Citation:||Journal of Neurotrauma, 2009; 26(8):A-54|
|Publisher:||Mary Ann Liebert|
|Conference Name:||Joint Symposium of The National and International Neurotrauma Societies (2nd : 2009 : Santa Barbara, California)|
|Levon Gabrielian, Stephen Helps, Jane Mathias, Robert Vink|
|Abstract:||Traumatic brain injury (TBI) remains a significant cause of death and disability in the community, thus representing an important and costly public health problem. Head injury often results in raised intracranial pressure (ICP) frequently coupled with secondary hypoxia. More than 50 percent of all deaths caused by TBI are related to secondary brain tissue oedema causing increased ICP and reduced cerebral perfusion pressure. To date, there is no effective pharmacological treatment for raised ICP after TBI, partly because widely used animal models of TBI may not replicate many of the physiological responses that are observed in human TBI. The aim of the current study was to investigate the ICP response in rats subjected to both fluid-percussion induced TBI alone and TBI coupled with secondary hypoxia. Adult male Sprague-Dawley rats (n=40) were subjected to brain trauma by lateral fluid percussion injury alone (2.6 atm), (n=5) or lateral fluid percussion injury coupled with secondary hypoxia (n=28) to simulate the effects of post-traumatic apnoea. Intracranial pressure was monitored using a Codman ICP Express monitor for 4h commencing 1–2 mins after TBI. To simulate the effects of post-traumatic apnoea, a subgroup of animals were subjected to 15min and 30min secondary hypoxia (8% and 11% O2 and 92% and 89% N2 accordingly) immediately after the trauma, and subsequently returned to normoxic conditions (30%O2 and 70%N2). TBI alone or coupled with hypoxia did not result in any significant increase of ICP in rats. However, a subgroup of rats with intracranial bleeding (mass lesions) showed some increase of ICP which varied depending on the level of intracranial bleeding. The presence of a mass lesion was critical for development of increased ICP in rats following TBI. Our results suggest that rats are a poor model for the characterization of ICP responses following TBI, and consequently inappropriate for the development of therapies targeting ICP. Although the reasons are currently unknown, we speculate that rats may be able to compensate for the intracranial expansion associated with cerebral oedema along their craniospinal axis. We therefore conclude that ICP responses after TBI, and the development of interventional therapies, should be explored in other species.|
|Description:||Abstracts from The Second Joint Symposium of The National and International Neurotrauma Societies, September 7–11, 2009 Santa Barbara, CA:A-54|
|Rights:||© Mary Ann Liebert, Inc.|
|Appears in Collections:||Aurora harvest 4|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.