Journal of neurotrauma
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Journal of neurotrauma · Jun 2002
Effects of mild hypothermia and alkalizing agents on brain injuries in rats with acute subdural hematomas.
Brain ischemia is the leading pathopysiological mechanism in the development of secondary brain damage after acute subdural hematoma (SDH). Hypothermia has been employed as an effective cerebroprotective treatment on brain injuries, but the control of the general condition is very difficult under hypothermia, and various severe complications have been reported. Cerebral acidosis in the ischemic area is one of the important factors augmenting the brain edema formation. ⋯ Furthermore, the volume of infarction at 24 h after the hematoma induction (54 +/- 3 mm(3); p < 0.01) was significantly smaller by the combined treatment compared with normothermia (70 +/- 2 mm(3)). The present findings indicate that mild hypothermia of 35 degrees C combined with THAM presents a potent cerebroprotective strategy. The protection of the BBB is one of the possible cerebroprotective mechanisms in this rat acute SDH model.
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Journal of neurotrauma · May 2002
Comparative StudyThe importance of brain temperature in patients after severe head injury: relationship to intracranial pressure, cerebral perfusion pressure, cerebral blood flow, and outcome.
Brain temperature was continuously measured in 58 patients after severe head injury and compared to rectal temperature, intracranial pressure, cerebral blood flow, and outcome after 3 months. The temperature difference between brain and rectal temperature was also calculated. Mild hypothermia (34-36 degrees C) was also used to treat uncontrollable intracranial pressure (ICP) above 20 mm Hg when other methods failed. ⋯ The lowest CBF was measured in patients with a brain temperature <36.0 degrees C and a negative brain-rectal temperature difference (17.1 +/- 14.0 mL/100 g/min). A positive trend for improved outcome was seen in patients with mild hypothermia. Simultaneous monitoring of brain and rectal temperature provides important diagnostic and prognostic information to guide the treatment of patients after severe head injury (SHI) and the wide differentials that can develop between the brain and core temperature, especially during rapid cooling, strongly supports the use of brain temperature measurement if therapeutic hypothermia is considered for head injury care.
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Journal of neurotrauma · May 2002
Caspase-3-mediated cleavage of amyloid precursor protein and formation of amyloid Beta peptide in traumatic axonal injury.
Immunohistochemical studies demonstrate accumulation of the beta-amyloid precursor protein (APP) within injured axons following traumatic brain injury (TBI). Despite such descriptions, little is known about the ultimate fate of accumulating APP at sites of traumatic axonal injury (TAI). Recently, caspase-3-mediated cleavage of APP and subsequent Abeta deposition was linked to apoptotic neuronal death pathways in hippocampal neurons following ischemic and excitotoxic brain injury. ⋯ Further, CMAP was colocalized with Abeta formation in foci of TAI. The current study demonstrates that caspase-3 cleavage of APP occurs in TAI and is associated with formation of Abeta peptide. These findings are of interest given recent epidemiological studies supporting an association between TBI and later risk for AD development.
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Journal of neurotrauma · May 2002
Cyclooxygenase-2 inhibition protects cultured cerebellar granule neurons from glutamate-mediated cell death.
Primary insults to the brain can initiate glutamate release that may result in excitotoxicity followed by neuronal cell death. This secondary process is mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA receptors in vivo and requires new gene expression. Neuronal cyclooxygenase-2 (COX2) expression is upregulated following brain insults, via glutamatergic and inflammatory mechanisms. ⋯ Approximately 50% protection from NMDA-mediated neurotoxicity, and no protection from kainate-mediated neurotoxicity was observed. Therefore, glutamate-mediated COX2 induction contributes to excitotoxic neuronal death. These results suggest that glutamate, NMDA, and kainate neurotoxicity involve distinct excitotoxic pathways, and that the glutamate and NMDA pathways may intersect at the level of COX2.
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Journal of neurotrauma · Apr 2002
Heme oxygenase-1 expression after spinal cord injury: the induction in activated neutrophils.
Tissue damage and neurological dysfunction after spinal cord injury may result, in part, from delayed or secondary mechanisms that appear to involve several endogenous factors. Among them, neutrophils are known to play important roles in the pathomechanisms of the secondary injury, that is, neutrophils are activated by an interaction with the endothelial cells, migrate into the damaged tissue and release several kinds of proteases or oxygen radicals. In the present study, we examined heme oxygenase-1 expression in the damaged spinal cord. ⋯ We found that many neutrophils expressing heme oxygenase-1 mRNA and protein were recruited into the damaged spinal cord with extensive hemorrhages during early stage of spinal cord injury. In an in vitro study, neutrophils incubated with proinflammatory cytokines, such as interleukin-1, 6 or interferon-gamma, expressed heme oxygenase-1 mRNA and protein. Based on these findings we conclude that the activated neutrophils can express heme oxygenase-1 in the injured spinal cord tissue, perhaps expecting modulatory and neuroprotective actions in the inflammatory response to spinal cord injury.