Journal of neurotrauma
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Journal of neurotrauma · Apr 2009
The temporal expression, cellular localization, and inhibition of the chemokines MIP-2 and MCP-1 after traumatic brain injury in the rat.
The expression of the neutrophil chemokine macrophage inflammatory protein-2 (MIP-2/CXCL2) and the monocyte chemokine monocyte chemotactic protein-1 (MCP-1/CCL2) have been described in glial cells in vitro but their origin following TBI has not been established. Furthermore, little is known of the modulation of these chemokines. Chemokine expression was investigated in male Sprague-Dawley rats following moderate lateral fluid percussion injury (LFPI). ⋯ MIP-2/CXCL2 and MCP-1/CCL2 are increased after injury, and neurons appear to be the source of this expression. Chemokine expression was selectively inhibited by dexamethasone. The implications of this are discussed.
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Spinal cord injury (SCI) launches a complex cascade of events that leads to progressive damage and loss of function. Compromise of plasma membrane integrity due to the mechanical impact is an acute event that may contribute to cellular dysfunction. Therefore, the objective of this study was to better understand the extent of acute plasma membrane damage associated with SCI as a function of injury severity and membrane defect size. ⋯ In addition, after moderate injury, cell bodies and axons (located up to 2 mm and 3 mm from the epicenter, respectively) took up significantly more of the 3-kDa and 10-kDa dextran permeability marker compared to sham controls. Permeable neuronal cell bodies exhibited a morphological appearance characterized by pericellular blebbing, suggesting that plasma membrane compromise is associated with pathophysiological cellular alterations. Collectively, these results enhance our understanding of acute SCI and provide targets for developing novel treatment strategies.
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Journal of neurotrauma · Mar 2009
Historical ArticleTherapeutic hypothermia: applications in pediatric cardiac arrest.
There is a rich history for the use of therapeutic hypothermia after cardiac arrest in neonatology and pediatrics. Laboratory reports date back to 1824 in experimental perinatal asphyxia. Similarly, clinical reports in pediatric cold water drowning victims represented key initiating work in the field. ⋯ Uncontrolled application (too deep and too long) and unique facets of asphyxial cardiac arrest in children (a very difficult insult to affect any benefit) likely combined to result in abandonment of therapeutic hypothermia in the mid to late 1980s. Important studies in perinatal medicine have built upon the landmark clinical trials in adults, and are once again bringing therapeutic hypothermia into standard care for pediatrics. Although more work is needed, particularly in the use of mild therapeutic hypothermia in children, there is a strong possibility that this important therapy will ultimately have broad applications after cardiac arrest and central nervous system (CNS) insults in the pediatric arena.
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Journal of neurotrauma · Mar 2009
Biography Historical ArticleTherapeutic hypothermia: the Safar vision.
At the 2(nd) International Brain Hypothermia conference, in Miami, the late Dr. Peter Safar was honored for his many contributions to the field of therapeutic hypothermia. ⋯ This review addresses key historical events in the development and implementation of therapeutic hypothermia across a number of central nervous system insults. A discussion of future potential uses of this therapy in a variety of applications as part of the Safar vision is also presented.
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Journal of neurotrauma · Mar 2009
ReviewManagement of pitfalls for the successful clinical use of hypothermia treatment.
Therapeutic hypothermia is a promising method for controlling intracranial pressure (ICP) in severely brain-injured patients. However, clinical data regarding the effect of brain hypothermia on overall outcome of these patients is limited. This may be because there are specific pitfalls associated with the clinical management of induced hypothermia in patients with severe traumatic brain injury (TBI). ⋯ For example, in our experience, posttraumatic hyperglycemia, exacerbated by cooling, may be ameliorated by the administration of a ketone body with mannitol. Prevention of selective free radical damage to neurons is also an important target for successful brain hypothermia treatment. Taken together, it is clear that several orchestrated steps should be initiated to enhance the protective effects of hypothermia therapy and prevent these possible pitfalls.