Journal of neurotrauma
-
Journal of neurotrauma · Aug 1994
Regional levels of free fatty acids and Evans blue extravasation after experimental brain injury.
The recently developed controlled cortical-impact (CCI) model of brain injury in rats serves as an excellent tool to understand some of the neurochemical mechanisms mediating the pathophysiology of traumatic brain injury. In this study, rats were subjected to lateral CCI brain injury of low-grade severity. Their brains were frozen in situ at various times after injury to measure regional levels of free fatty acids. ⋯ Extravasation of Evans blue was found to be significantly increased in the ipsilateral cortex of injured animals at 30 min and 10 h after brain injury. These results indicate the degradation of membrane phospholipids and blood-brain barrier breakdown in the ipsilateral cortex after lateral CCI brain injury. These results also suggest that arachidonic acid and its metabolites may play a role as a mediator in the blood-brain barrier breakdown associated with cortical impact brain injury in rats.
-
Journal of neurotrauma · Aug 1994
Direct measurement of hydroxyl radicals, lipid peroxidation, and blood-brain barrier disruption following unilateral cortical impact head injury in the rat.
We present data correlating the time courses of hydroxyl radical (. OH) production, lipid peroxidation, and blood-brain barrier (BBB) damage following unilateral head injury in the rat. Using a controlled cortical impact device to inflict head injury, we have directly measured brain. ⋯ The results suggest that there is an immediate, posttraumatic burst in. OH formation, followed by a progressive increase in lipid peroxidation and a similar, although slightly delayed, time-related opening of the BBB. The attenuation of BBB damage by U-74006F suggests that this chain of events can be interrupted by administration of an antioxidant/lipid peroxidation inhibitor.
-
Journal of neurotrauma · Jun 1994
Increased anticholinergic sensitivity following closed skull impact and controlled cortical impact traumatic brain injury in the rat.
Evidence suggests that prolonged memory deficits in several neurodegenerative diseases are attributable to deficits in central cholinergic neurotransmission. In traumatic brain injury (TBI), such cholinergic deficits also may contribute to prolonged memory disturbances. This study determined whether moderate magnitudes of TBI produced by controlled cortical impact and mild magnitudes of experimental TBI produced by a new closed head impact technique in rats would produce an enhanced vulnerability to the memory disruptive effects of scopolamine, a muscarinic cholinergic receptor antagonist. ⋯ These data demonstrate that covert deficits can persist after the recovery of normal function. These deficits may be attributable to a decrease in the ability of cholinergic neurons to function properly. These data also provide important insights into features of receptor-coupled disturbances that could contribute to the maintenance of enduring cognitive deficits following TBI.
-
Journal of neurotrauma · Jun 1994
Early microvascular and neuronal consequences of traumatic brain injury: a light and electron microscopic study in rats.
The purpose of this study was to document the early morphologic consequences of moderate traumatic brain injury (TBI) in anesthetized Sprague-Dawley rats. Normothermic rats (37 degrees C) were injured with a fluid percussion pulse (1.7-2.1 atm) administered by an injury cannula positioned parasagittally over the right cerebral cortex (n = 7). At 45 min following TBI, rats were injected with the protein tracer horseradish peroxidase (HRP) and perfusion fixed or immersion fixed 15 min later for light and electron microscopic analysis. ⋯ In nonperfused traumatized rats, luminal platelet aggregates were also detected at sites of hemorrhage. In this model of TBI, a consistent pattern of microvascular and neuronal abnormalities can be documented in the early posttraumatic period. Pathomechanisms underlying these early changes are discussed in terms of primary and secondary injury processes.
-
Journal of neurotrauma · Jun 1994
The efficacy of barbiturate coma in the management of uncontrolled intracranial hypertension following neurosurgical trauma.
The purpose of this study was to evaluate the role of barbiturate therapy as an adjunctive treatment for control of intracranial hypertension when conventional methods failed. To this end, a retrospective chart review was conducted on 21 neurosurgical trauma patients with uncontrolled intracranial pressure (ICP) admitted to a trauma/intensive care unit. ⋯ The survival of patients experiencing ICP control with barbiturate coma was better than those patients who failed therapy (71% vs 14%, p = 0.021). Thus, in a subgroup of neurosurgical trauma patients who are refractory to conventional management of elevated ICP, barbiturates appear to improve survival, suggesting that this therapy has an important role in the management of neurotrauma patients.