Journal of neurotrauma
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Journal of neurotrauma · May 2000
Three months of chronic ethanol administration and the behavioral outcome of rats after lateral fluid percussion brain injury.
This study examined the effects of 3 months of chronic ethanol administration (CEAn) on the behavioral outcome in rats after lateral fluid percussion (FP) brain injury. Rats were given either an ethanol liquid diet (ethanol diet groups) or a pair-fed isocaloric sucrose control diet (control diet groups) for 3 months. Then, rats from both diet groups were subjected to either lateral FP brain injury of moderate severity (1.8 atm) or to sham operation. ⋯ However, a trend towards cognitive impairment in the sham animals and a trend towards reduced deficits in the brain-injured animals were observed in the ethanol diet group. Histologic analysis of injured animals from both diet groups revealed similar extents of ipsilateral cortical and hippocampal CA3 damage. These results, in general, suggest that 3 months of CEAn does not significantly alter the behavioral and morphologic outcome of experimental brain injury.
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Journal of neurotrauma · May 2000
Comparative StudyEarly predictors of mortality and morbidity after severe closed head injury.
Mortality and morbidity of 158 patients with severe head injury were studied in relation to age, and early (24-h) clinical and computed tomography data. For comparison of outcome data in survivors, a group of 32 patients with traumatic injuries to parts of the body other than the head was used as controls. Within the head-injured group, the mortality rate was 51%. ⋯ They also report more quality of life-related functional limitations on the SIP scales for mobility, intellectual behavior, communication, home management, eating, and work. Linear regression analysis resulted in age being the only important predictor of outcome on the GOS, the GCS score being the best predictor of neuropsychological functioning, and pupillary reactivity being the most predictive for self-reported quality of life as measured by SIP. Those factors important for predicting mortality (clinical variables such as ICP or blood glucose level, and CT observations) failed to show any significant relationship with morbidity.
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Journal of neurotrauma · May 2000
Astrocytes generate isoprostanes in response to trauma or oxygen radicals.
Previous studies have shown that oxygen radical scavengers prevent the reduced cerebral blood flow that occurs following experimental traumatic brain injury. The exact chemical species responsible for the posttraumatic reduction in flow is unknown. We tested whether isoprostanes, which are formed by non-cyclooxygenase-dependent free radical attack of arachidonic acid and are vasoconstrictors of the cerebral circulation, are increased in astrocytes following stretch-induced trauma or injury with a free radical generating system. ⋯ The hydroxyl generating system caused free and cell-bound isoprostanes to increase to more than 400% of control. After trauma, free and membrane bound isoprostanes increased to 321 +/- 34% and 229 +/- 23% of control, respectively, and posttraumatic increases were prevented by deferoxamine. Since astrocytes are in close proximity to cerebral vessels, posttraumatic free radical formation may increase the formation of isoprostanes, which in turn produce vasoconstriction and decrease cerebral blood flow.
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Journal of neurotrauma · Apr 2000
Ethanol reduces metabolic uncoupling following experimental head injury.
Previous investigations have shown that ethanol is neuroprotective following experimental traumatic brain injury (TBI). This study sought to determine if the neuroprotective effects of ethanol in a controlled cortical impact (CCI) injury model are related to its effects on cerebral glucose metabolism and blood flow. Adult rats were given ethanol (1.0 g/kg) or saline by intraperitoneal injection followed 40 min later by injury. ⋯ Simultaneously, the reduction in CBF typically seen within the contusion core and penumbra after CCI is less severe when ethanol is present. The net effect of these changes is a decreased degree of uncoupling between glucose metabolism and CBF that otherwise occurs in the absence of ethanol. These changes may likely explain the neuroprotective effect of ethanol.
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Journal of neurotrauma · Mar 2000
Effects of hypothermia on intracranial pressure and brain edema formation: studies in a rat acute subdural hematoma model.
Acute subdural hematoma (SDH) is the most common mass lesion in severe head injury, and brain ischemia is the leading pathophysiological mechanism in the development of secondary brain damage following SDH. Hypothermia has been employed as an effective neuroprotective procedure in clinical and laboratory studies on cerebral ischemic and contusional injuries. In the present study, we used a rat acute SDH model to assess the effect of hypothermia on the intracranial pressure (ICP) and also on the brain edema formation at 4 h after hematoma induction. ⋯ This reduction in brain edema formation was comparable to the results of MK-801 treatment (80.95 +/- 0.35%, p<0.01). The present findings indicate that hypothermia represents a potent neuroprotective strategy. The possible protective mechanisms of hypothermic protection afforded in this rat acute SDH model are discussed.