Journal of neurotrauma
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Journal of neurotrauma · Jan 2000
Clinical TrialCerebral hemodynamic effects of 7.2% hypertonic saline in patients with head injury and raised intracranial pressure.
The aim of the present study was to investigate the acute effects of 7.2% hypertonic saline (HS) on intracranial pressure (ICP), cerebral and systemic hemodynamics, serum sodium, and osmolality in 14 patients with moderate and severe traumatic brain injury (Glasgow Coma Scale < or =13) and raised ICP (>15 mm Hg) within the first 72 h postinjury. After CO2 reactivity and autoregulation were tested, each patient received a 15-min infusion of 7.2% HS (1,232 mEq/L, volume 1.5 mL/kg). ICP, serial hemodynamics, cerebral blood flow (CBF) estimated from cerebral arteriovenous oxygen content difference (AVDO2), and laboratory variables, including serum osmolality, electrolytes, urea, and creatinine were collected before infusion (T0) and at 5, 30, 60, and 120 min after (T5, T30, T60, T120). ⋯ A significant positive correlation (r = 0.75; p = 0.02) between ICP and serum osmolality was found at T5. The administration of 7.2% HS in patients with traumatic brain injury significantly reduces ICP without significant changes in relative global CBF (expressed as 1/AVDO2), increases CI and transiently increases PAOP, without changing MABP and urine output. The correlation between changes in osmolality and ICP supports the hypothesis that HSS may in part decrease ICP by means of an osmotic mechanism.
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Journal of neurotrauma · Jan 2000
Extracellular N-acetyl-aspartate as a biochemical marker of the severity of neuronal damage following experimental acute traumatic brain injury.
We evaluated the acute changes in interstitial and whole brain N-acetyl-aspartate (NAA) measured by high-performance liquid chromatography in animal models of isolated traumatic brain injury (TBI) and TBI combined with secondary insult (hypotension-hypoxia [HH]). The Marmarou impact-acceleration model was used. Four groups were studied: (1) sham-operated control, (2) TBI alone (TBI 500 gm, 2 m), (3) TBI plus 30 min of hypoxia (PaO2, approximately 40 mm Hg) and hypotension (mean arterial blood pressure, approximately 40 mm Hg) (THH), and (4) HH alone. ⋯ The whole brain NAA (NAAw) concentration in controls was 8.5+/-0.5 mmol/kg wet weight. There was no significant difference between TBI and controls; however, there was a significant decrease in NAAw in the THH and HH group compared to controls. Thus, in this animal model of TBI and TBI with secondary insult, we found that persistent, marked elevation in NAA is associated with TBI and secondary ischemic/hypoxic insult, but not with isolated TBI alone.
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Journal of neurotrauma · Jan 2000
Application of 2,3,5-triphenyltetrazolium chloride staining to evaluate injury volume after controlled cortical impact brain injury: role of brain edema in evolution of injury volume.
A reliable method for measuring injury volume after traumatic brain injury (TBI) is of great importance when studying pharmacological protective agents in the field of head trauma research. Utilization of 2,3,5-triphenyltetrazolium chloride (TTC) has gained extensive acceptance in stroke research and has recently been applied to injury volume measurement in the lateral fluid percussion model. The present study was undertaken to apply this method to the controlled cortical impact (CCI) model and to study the role of brain edema. ⋯ A statistically significant reduction of injury volume was observed after postinjury day 4. We also observed that due to the presence of brain edema absolute injury volume is more than corrected injury volume in the first 3 days after injury as opposed to injury volume at postinjury day 7. These results suggest that the measurement of injury volume with TTC staining should be corrected for brain edema in the CCI brain injury model.
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Journal of neurotrauma · Jan 2000
Comparative StudyFluid percussion injury transiently increases then decreases brain oxygen consumption in the rat.
The oxygen consumption (VO2 microL/h/mg) of sham and of traumatized rat brains within 30 min and 6 h after a lateral fluid percussion injury (FPI) was measured with the Cartesian microrespirometer. Brain slices were cut at the plain of injury and site-specific 20-60-microg cores of tissue were transferred to the microrespirometer. In sham brains, the cortical VO2 (CVO2) was 13.78+/-0.64 and the hippocampal VO2 (HPVO2) was 11.20+/-0.58 microL/h/mg (p<0.05). ⋯ The data indicate that normal CVO2 is greater than normal HPVO2. The FPI produces significant increases in both CVO2 and HPVO2. Also, while the immediate increase in CVO2 appears to be injury-site dependent, that is, regional, the increase in HPVO2 appears to be global.
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Journal of neurotrauma · Dec 1999
Chronic and acute compressive spinal cord lesions in dogs due to intervertebral disc herniation are associated with elevation in lumbar cerebrospinal fluid glutamate concentration.
Acute injury to the central nervous system initiates a series of biochemical events that cause secondary tissue damage. The accumulation of excessive concentrations of glutamate in the extracellular space causes excitotoxic damage, and is incriminated as a mediator of this secondary tissue damage. The aim of this study was to measure the concentration of glutamate in cerebrospinal fluid (CSF) obtained from the cerebellomedullary cistern and lumbar subarachnoid space in dogs with acute and chronic compressive injuries of the cervical and thoracolumbar spinal cord, and to correlate the glutamate concentration with injury severity. ⋯ However, dogs with severe, acute thoracolumbar disc herniations have two- to 10-fold increases in glutamate concentration in their lumbar CSF at intervals of >12 h after injury. Moreover, the severity of their clinical signs is directly related to the glutamate concentration. Dogs with chronic compressive thoracolumbar lesions have a two-fold elevation of CSF glutamate concentration, suggesting that excitotoxicity may also be a component of chronic spinal cord compression.