Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2000
Increased adrenomedullin in cerebrospinal fluid after traumatic brain injury in children: a preliminary report.
Adrenomedullin is a recently discovered 52-amino-acid peptide that is a potent vasodilator. Infusion of adrenomedullin increases regional cerebral blood flow and reduces infarct volume after vascular occlusion in rats. Adrenomedullin may represent an endogenous neuroprotectant since it is increased after focal brain ischemia. ⋯ All 36 case samples had an adrenomedullin concentration above the median value for the controls (1.52 fmol/ml). We conclude adrenomedullin is elevated in the CSF of children following severe TBI. We speculate that it participates in the endogenous response to cerebral hypoperfusion after TBI.
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Acta Neurochir. Suppl. · Jan 2000
The permissive nature of blood brain barrier (BBB) opening in edema formation following traumatic brain injury.
The contribution of blood brain barrier opening to traumatic brain edema is not known. This study compares the course of traumatic BBB disruption and edema formation, with the hypothesis that they are not obligately related. Sprague-Dawley rats were divided into three groups: Group A (n = 47)--Impact Acceleration (IAM); Group B (n = 104)--lateral cortical impact (CCI); Group C (n = 26)--IAM + hypoxia & hypotension (THH). ⋯ Edema formation clearly does not correspond with BBB opening and an open BBB is clearly not required for edema formation. However we hypothesize that a permeable BBB permissively worsens the process, by acting as a low resistance pathway for ion and water movement. These findings are consistent with our general hypothesis that edema formation after TBI is mainly cytotoxic.
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Acta Neurochir. Suppl. · Jan 2000
Time profile of neuron specific enolase serum levels after experimental brain injury in rat.
The aim of this study was to investigate the time course of NSE serum levels after traumatic brain injury in rats. 65 male Wistar rats were subjected to severe cortical impact injury (100 PSI, 2 mm deformation). Blood samples were drawn directly after trauma, after 1 h, 6 h, 12 h, 24 h, and 48 h in the trauma group as well as in sham operated animals directly after craniotomy, after 6 h and after 48 h. NSE serum levels were estimated with a commercially available enzyme immuno assay (LIA-mat Sangtec). ⋯ We demonstrated a time dependent release of NSE into the serum after trauma. The highest NSE serum values were detected six hours after trauma (31.5 micrograms/l, mean, n = 10). NSE serum level seems to reflect neuronal damage after cortical contusion in the rat in a time dependent manner.
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Acta Neurochir. Suppl. · Jan 2000
Effects of hypothermia on intracranial hemodynamics and ischemic brain damage-studies in the rat acute subdural hematoma model.
Brain ischemia is the leading pathophysiological mechanism in the development of secondary brain damage after subdural hematoma (SDH). Hypothermia has been used as the effective neuroprotective treatment in clinical and laboratory studies of ischemic brain injury. In this study, we have examined the rat acute SDH model to assess the effect of hypothermia upon intracranial hemodynamics and also upon ischemic brain injury 4 hours after the induction of hematoma. ⋯ This reduction in brain edema formation was comparable to the result of MK-801 (2 mg/kg) treatment (80.95 +/- 0.35%; p < 0.01). Ischemic brain damage detected by H-E staining was also significantly reduced in the hypothermia and MK-801 treated groups (59.1 +/- 12.3 mm3 and 66.4 +/- 13.8 mm3; p < 0.01 and p < 0.05) compared with the normothermic control group (86.6 +/- 20.7 mm3). In conclusion, the present study demonstrates that hypothermia is a potent neuroprotective method and an inhibition of the glutamate excitotoxic process may contribute the protective mechanisms of hypothermia in this rat acute SDH model.
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Acta Neurochir. Suppl. · Jan 2000
The effects of dopamine on edema formation in two models of traumatic brain injury.
The risk of vasopressors worsening cerebral edema has been raised. Previously we have reported that dopamine was able to restore cerebral blood flow in a model of monotonically rising intracranial pressure. In this study the effects of dopamine on cortical contusion and diffuse injury with secondary insult are examined. ⋯ Dopamine however significantly worsened edema in ipsilateral and contralateral hippocampus and both temporal cortices. ADC remained unchanged except in the contralateral hippocampus where both water content and ADC rose with dopamine suggesting precipitation of a vasogenic edema. In this study dopamine clearly worsened edema formation in two models of traumatic brain injury, and we conclude that there may be analogous clinical situations; therefore pressors should not be considered a 'blanket' therapy for all patients with a low cerebral perfusion pressure.