Articles: brain-injuries.
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Journal of neurotrauma · Oct 2016
Retracted PublicationNorepinephrine Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis after Traumatic Brain Injury via Block of ERK MAPK and IL-6 in Juvenile Pigs.
Traumatic brain injury (TBI) contributes to morbidity in children, and boys are disproportionately represented. Cerebral autoregulation is impaired after TBI, contributing to poor outcome. Cerebral perfusion pressure (CPP) is often normalized by use of vasoactive agents to increase mean arterial pressure (MAP). ⋯ NE attenuated loss of neurons in CA1 and CA3 hippocampus of males and females after FPI. These data indicate that NE protects autoregulation and limits hippocampal neuronal cell necrosis via blockade of ERK and IL-6 after FPI in both male and female juvenile pigs. These data suggest that use of NE to improve outcome after TBI is both sex and age dependent.
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Pediatr Crit Care Me · Mar 2016
Retracted PublicationPreferential Protection of Cerebral Autoregulation and Reduction of Hippocampal Necrosis With Norepinephrine After Traumatic Brain Injury in Female Piglets.
Traumatic brain injury contributes to morbidity in children and boys is disproportionately represented. Cerebral autoregulation is impaired after traumatic brain injury, contributing to poor outcome. Cerebral perfusion pressure is often normalized by the use of vasopressors to increase mean arterial pressure. In prior studies, we observed that phenylephrine prevented impairment of autoregulation in female but exacerbated in male piglets after fluid percussion injury. In contrast, dopamine prevented impairment of autoregulation in both sexes after fluid percussion injury, suggesting that pressor choice impacts outcome. The extracellular signal-regulated kinase isoform of mitogen-activated protein kinase produces hemodynamic impairment after fluid percussion injury, but the role of the cytokine interleukin-6 is unknown. We investigated whether norepinephrine sex-dependently protects autoregulation and limits histopathology after fluid percussion injury and the role of extracellular signal-regulated kinase and interleukin-6 in that outcome. ⋯ Norepinephrine protects autoregulation and limits hippocampal neuronal cell necrosis via modulation of extracellular signal-regulated kinase mitogen-activated protein kinase and interleukin-6 after fluid percussion injury in a sex-dependent manner.
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Critical care medicine · Mar 2012
Retracted PublicationProtective effects of melanocortins on short-term changes in a rat model of traumatic brain injury*.
Treatment for traumatic brain injury remains elusive despite compelling evidence from animal models for a variety of therapeutic targets. Melanocortins have established neuroprotective effects against experimental ischemic stroke. We investigated whether melanocortin treatment of traumatic brain injury induces neuroprotection and promotes functional recovery. ⋯ Our data indicate that melanocortins protect against traumatic brain injury, in a broad time window and through activation of MC4 receptors, by counteracting the main traumatic brain injury-related mechanisms of damage. These findings could have major clinical implications.
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Retracted Publication
Kynurenate attenuates the accumulation of diacylglycerol and free fatty acids after experimental brain injury in the rat.
This study examined the effects of the administration of kynurenate, a non-specific excitatory amino acid (EAA) receptor subtype antagonist, on the regional accumulation of diacylglycerol (DG) and free fatty acids (FFAs) after lateral fluid percussion (FP) brain injury in the rat. After brain injury of moderate severity (2.0 atm), rats were treated with either kynurenate (200 mg/kg, i.v.) or saline at 5 min after injury. In the saline-treated brain-injured rats, levels of all individual DG-fatty acids (palmitic, stearic, oleic and arachidonic acids) and total DG-fatty acids were increased in the ipsilateral left cortex and hippocampus at 30 min and 60 min after injury. ⋯ Kynurenate administration attenuated increases of all individual and total FFAs in the ipsilateral cortex and hippocampus either at 30 min alone or at both 30 min and 60 min after FP brain injury. In the contralateral cortex, levels of both DG-fatty acids and FFAs were not increased in the saline-treated injured rats and were also not affected by the administration of kynurenate. These results support the role of EAA receptor subtypes in the phospholipases-catalyzed formation of DG and FFAs in the ipsilateral cortex and hippocampus after lateral FP brain injury.