Traumatic Brain Injury

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Pierre Bouzat - One of the best experts on this subject based on the ideXlab platform.

  • mannitol improves Brain tissue oxygenation in a model of diffuse Traumatic Brain Injury
    Critical Care Medicine, 2015
    Co-Authors: C Schilte, Pierre Bouzat, A Millet, Karin Pernetgallay, P Boucheix, Benjamin Lemasson, Emmanuel L Barbier, Jean Francois Payen
    Abstract:

    OBJECTIVES: Based on evidence supporting a potential relation between postTraumatic Brain hypoxia and microcirculatory derangements with cell edema, we investigated the effects of the antiedematous agent mannitol on Brain tissue oxygenation in a model of diffuse Traumatic Brain Injury. DESIGN: Experimental study. SETTING: Neurosciences and physiology laboratories. SUBJECTS: Adult male Wistar rats. INTERVENTIONS: Thirty minutes after diffuse Traumatic Brain Injury (impact-acceleration model), rats were IV administered with either a saline solution (Traumatic Brain Injury-saline group) or 20% mannitol (1 g/kg) (Traumatic Brain Injury-mannitol group). Sham-saline and sham-mannitol groups received no insult. MEASUREMENTS AND MAIN RESULTS: Two series of experiments were conducted 2 hours after Traumatic Brain Injury (or equivalent) to investigate 1) the effect of mannitol on Brain edema and oxygenation, using a multiparametric magnetic resonance-based approach (n = 10 rats per group) to measure the apparent diffusion coefficient, tissue oxygen saturation, mean transit time, and blood volume fraction in the cortex and caudoputamen; 2) the effect of mannitol on Brain tissue PO2 and on venous oxygen saturation of the superior sagittal sinus (n = 5 rats per group); and 3) the cortical ultrastructural changes after treatment (n = 1 per group, taken from the first experiment). Compared with the sham-saline group, the Traumatic Brain Injury-saline group had significantly lower tissue oxygen saturation, Brain tissue PO2, and venous oxygen saturation of the superior sagittal sinus values concomitant with diffuse Brain edema. These effects were associated with microcirculatory collapse due to astrocyte swelling. Treatment with mannitol after Traumatic Brain Injury reversed all these effects. In the absence of Traumatic Brain Injury, mannitol had no effect on Brain oxygenation. Mean transit time and blood volume fraction were comparable between the four groups of rats. CONCLUSION: The development of postTraumatic Brain edema can limit the oxygen utilization by Brain tissue without evidence of Brain ischemia. Our findings indicate that an antiedematous agent such as mannitol can improve Brain tissue oxygenation, possibly by limiting astrocyte swelling and restoring capillary perfusion.

  • changes in Brain tissue oxygenation after treatment of diffuse Traumatic Brain Injury by erythropoietin
    Critical Care Medicine, 2013
    Co-Authors: Pierre Bouzat, A Millet, Yvonnick Boue, Karin Pernetgallay, Thibaut Trouvebuisson, Lucie Gaidechevronnay
    Abstract:

    OBJECTIVES: To investigate the effects of recombinant human erythropoietin on Brain oxygenation in a model of diffuse Traumatic Brain Injury. DESIGN: Adult male Wistar rats. SETTING: Neurosciences and physiology laboratories. INTERVENTIONS: Thirty minutes after diffuse Traumatic Brain Injury (impact-acceleration model), rats were intravenously administered with either a saline solution or a recombinant human erythropoietin (5000 IU/kg). A third group received no Traumatic Brain Injury insult (sham-operated). MEASUREMENTS AND MAIN RESULTS: Three series of experiments were conducted 2 hours after Traumatic Brain Injury to investigate: 1) the effect of recombinant human erythropoietin on Brain edema using diffusion-weighted magnetic resonance imaging and measurements of apparent diffusion coefficient (n = 11 rats per group); local Brain oxygen saturation, mean transit time, and blood volume fraction were subsequently measured using a multiparametric magnetic resonance-based approach to estimate Brain oxygenation and Brain perfusion in the neocortex and caudoputamen; 2) the effect of recombinant human erythropoietin on Brain tissue PO₂ in similar experiments (n = 5 rats per group); and 3) the cortical ultrastructural changes after treatment (n = 1 rat per group). Compared with the sham-operated group, Traumatic Brain Injury saline rats showed a significant decrease in local Brain oxygen saturation and in Brain tissue PO₂ alongside Brain edema formation and microvascular lumen collapse at H2. Treatment with recombinant human erythropoietin reversed all of these Traumatic Brain Injury-induced changes. Brain perfusion (mean transit time and blood volume fraction) was comparable between the three groups of animals. CONCLUSION: Our findings indicate that Brain hypoxia can be related to microcirculatory derangements and cell edema without evidence of Brain ischemia. These changes were reversed with post-Traumatic administration of recombinant human erythropoietin, thus offering new perspectives in the use of this drug in Brain Injury.

  • reduced Brain edema and functional deficits after treatment of diffuse Traumatic Brain Injury by carbamylated erythropoietin derivative
    Critical Care Medicine, 2011
    Co-Authors: Pierre Bouzat, Emmanuel L Barbier, Gilles Francony, Sebastien Thomas, Samuel Valable, Franck Mauconduit, M C Fevre, Myriam Bernaudin, Hana Lahrech, Jean Francois Payen
    Abstract:

    OBJECTIVE: To investigate the effects of carbamylated erythropoietin, a modified erythropoietin lacking erythropoietic activity, on Brain edema and functional recovery in a model of diffuse Traumatic Brain Injury. DESIGN: Adult male Wistar rats. SETTING: Neurosciences and physiology laboratories. INTERVENTIONS: Thirty minutes after diffuse Traumatic Brain Injury (impact-acceleration model), rats were intravenously administered with either a saline solution (Traumatic Brain Injury-saline) or carbamylated erythropoietin (50 μg/kg; Traumatic Brain Injury-carbamylated erythropoietin). A third group received no Traumatic Brain Injury insult (sham-operated). MEASUREMENTS AND MAIN RESULTS: Three series of experiments were conducted to investigate: 1) the effect of carbamylated erythropoietin on Brain edema before and 1 hr after Traumatic Brain Injury using diffusion-weighted magnetic resonance imaging and measurements of apparent diffusion coefficient (n = 10 rats per group), and the phosphorylation level of Brain extracellular-regulated kinase-1/-2 was also determined to indicate the presence of an activated cell signaling pathway; 2) the time course of Brain edema using magnetic resonance imaging between 4 and 6 hrs postInjury and the gravimetric technique at 6 hrs (n = 10 rats per group); and 3) motor and cognitive function over 10 days post Traumatic Brain Injury, testing acute somatomotor reflexes, adhesive paper removal, and two-way active avoidance (n = 8 rats per group). Compared to Traumatic Brain Injury-saline rats, rats receiving Traumatic Brain Injury-carbamylated erythropoietin showed a significant reduction in Brain edema formation at 1 hr that was sustained until 6 hrs when results were comparable with sham-operated rats. This antiedematous effect of carbamylated erythropoietin was possibly mediated through an early inhibition of extracellular-regulated kinase-1/-2 phosphorylation. Compared to Traumatic Brain Injury-saline rats, Traumatic Brain Injury-carbamylated erythropoietin rats showed improved functional recovery of the acute somatomotor reflexes post Traumatic Brain Injury, took less time to remove adhesive from the forelimbs, and showed higher percentages of correct avoidance responses. CONCLUSION: Our findings indicate that early postTraumatic administration of carbamylated erythropoietin reduces Brain edema development until at least 6 hrs postInjury and improves neurologic recovery. Carbamylated erythropoietin can thus be considered as a potential agent in the treatment of Traumatic Brain Injury-induced diffuse edema.

Linda J Carroll - One of the best experts on this subject based on the ideXlab platform.

Lucie Gaidechevronnay - One of the best experts on this subject based on the ideXlab platform.

  • changes in Brain tissue oxygenation after treatment of diffuse Traumatic Brain Injury by erythropoietin
    Critical Care Medicine, 2013
    Co-Authors: Pierre Bouzat, A Millet, Yvonnick Boue, Karin Pernetgallay, Thibaut Trouvebuisson, Lucie Gaidechevronnay
    Abstract:

    OBJECTIVES: To investigate the effects of recombinant human erythropoietin on Brain oxygenation in a model of diffuse Traumatic Brain Injury. DESIGN: Adult male Wistar rats. SETTING: Neurosciences and physiology laboratories. INTERVENTIONS: Thirty minutes after diffuse Traumatic Brain Injury (impact-acceleration model), rats were intravenously administered with either a saline solution or a recombinant human erythropoietin (5000 IU/kg). A third group received no Traumatic Brain Injury insult (sham-operated). MEASUREMENTS AND MAIN RESULTS: Three series of experiments were conducted 2 hours after Traumatic Brain Injury to investigate: 1) the effect of recombinant human erythropoietin on Brain edema using diffusion-weighted magnetic resonance imaging and measurements of apparent diffusion coefficient (n = 11 rats per group); local Brain oxygen saturation, mean transit time, and blood volume fraction were subsequently measured using a multiparametric magnetic resonance-based approach to estimate Brain oxygenation and Brain perfusion in the neocortex and caudoputamen; 2) the effect of recombinant human erythropoietin on Brain tissue PO₂ in similar experiments (n = 5 rats per group); and 3) the cortical ultrastructural changes after treatment (n = 1 rat per group). Compared with the sham-operated group, Traumatic Brain Injury saline rats showed a significant decrease in local Brain oxygen saturation and in Brain tissue PO₂ alongside Brain edema formation and microvascular lumen collapse at H2. Treatment with recombinant human erythropoietin reversed all of these Traumatic Brain Injury-induced changes. Brain perfusion (mean transit time and blood volume fraction) was comparable between the three groups of animals. CONCLUSION: Our findings indicate that Brain hypoxia can be related to microcirculatory derangements and cell edema without evidence of Brain ischemia. These changes were reversed with post-Traumatic administration of recombinant human erythropoietin, thus offering new perspectives in the use of this drug in Brain Injury.

Jean Francois Payen - One of the best experts on this subject based on the ideXlab platform.

  • mannitol improves Brain tissue oxygenation in a model of diffuse Traumatic Brain Injury
    Critical Care Medicine, 2015
    Co-Authors: C Schilte, Pierre Bouzat, A Millet, Karin Pernetgallay, P Boucheix, Benjamin Lemasson, Emmanuel L Barbier, Jean Francois Payen
    Abstract:

    OBJECTIVES: Based on evidence supporting a potential relation between postTraumatic Brain hypoxia and microcirculatory derangements with cell edema, we investigated the effects of the antiedematous agent mannitol on Brain tissue oxygenation in a model of diffuse Traumatic Brain Injury. DESIGN: Experimental study. SETTING: Neurosciences and physiology laboratories. SUBJECTS: Adult male Wistar rats. INTERVENTIONS: Thirty minutes after diffuse Traumatic Brain Injury (impact-acceleration model), rats were IV administered with either a saline solution (Traumatic Brain Injury-saline group) or 20% mannitol (1 g/kg) (Traumatic Brain Injury-mannitol group). Sham-saline and sham-mannitol groups received no insult. MEASUREMENTS AND MAIN RESULTS: Two series of experiments were conducted 2 hours after Traumatic Brain Injury (or equivalent) to investigate 1) the effect of mannitol on Brain edema and oxygenation, using a multiparametric magnetic resonance-based approach (n = 10 rats per group) to measure the apparent diffusion coefficient, tissue oxygen saturation, mean transit time, and blood volume fraction in the cortex and caudoputamen; 2) the effect of mannitol on Brain tissue PO2 and on venous oxygen saturation of the superior sagittal sinus (n = 5 rats per group); and 3) the cortical ultrastructural changes after treatment (n = 1 per group, taken from the first experiment). Compared with the sham-saline group, the Traumatic Brain Injury-saline group had significantly lower tissue oxygen saturation, Brain tissue PO2, and venous oxygen saturation of the superior sagittal sinus values concomitant with diffuse Brain edema. These effects were associated with microcirculatory collapse due to astrocyte swelling. Treatment with mannitol after Traumatic Brain Injury reversed all these effects. In the absence of Traumatic Brain Injury, mannitol had no effect on Brain oxygenation. Mean transit time and blood volume fraction were comparable between the four groups of rats. CONCLUSION: The development of postTraumatic Brain edema can limit the oxygen utilization by Brain tissue without evidence of Brain ischemia. Our findings indicate that an antiedematous agent such as mannitol can improve Brain tissue oxygenation, possibly by limiting astrocyte swelling and restoring capillary perfusion.

  • reduced Brain edema and functional deficits after treatment of diffuse Traumatic Brain Injury by carbamylated erythropoietin derivative
    Critical Care Medicine, 2011
    Co-Authors: Pierre Bouzat, Emmanuel L Barbier, Gilles Francony, Sebastien Thomas, Samuel Valable, Franck Mauconduit, M C Fevre, Myriam Bernaudin, Hana Lahrech, Jean Francois Payen
    Abstract:

    OBJECTIVE: To investigate the effects of carbamylated erythropoietin, a modified erythropoietin lacking erythropoietic activity, on Brain edema and functional recovery in a model of diffuse Traumatic Brain Injury. DESIGN: Adult male Wistar rats. SETTING: Neurosciences and physiology laboratories. INTERVENTIONS: Thirty minutes after diffuse Traumatic Brain Injury (impact-acceleration model), rats were intravenously administered with either a saline solution (Traumatic Brain Injury-saline) or carbamylated erythropoietin (50 μg/kg; Traumatic Brain Injury-carbamylated erythropoietin). A third group received no Traumatic Brain Injury insult (sham-operated). MEASUREMENTS AND MAIN RESULTS: Three series of experiments were conducted to investigate: 1) the effect of carbamylated erythropoietin on Brain edema before and 1 hr after Traumatic Brain Injury using diffusion-weighted magnetic resonance imaging and measurements of apparent diffusion coefficient (n = 10 rats per group), and the phosphorylation level of Brain extracellular-regulated kinase-1/-2 was also determined to indicate the presence of an activated cell signaling pathway; 2) the time course of Brain edema using magnetic resonance imaging between 4 and 6 hrs postInjury and the gravimetric technique at 6 hrs (n = 10 rats per group); and 3) motor and cognitive function over 10 days post Traumatic Brain Injury, testing acute somatomotor reflexes, adhesive paper removal, and two-way active avoidance (n = 8 rats per group). Compared to Traumatic Brain Injury-saline rats, rats receiving Traumatic Brain Injury-carbamylated erythropoietin showed a significant reduction in Brain edema formation at 1 hr that was sustained until 6 hrs when results were comparable with sham-operated rats. This antiedematous effect of carbamylated erythropoietin was possibly mediated through an early inhibition of extracellular-regulated kinase-1/-2 phosphorylation. Compared to Traumatic Brain Injury-saline rats, Traumatic Brain Injury-carbamylated erythropoietin rats showed improved functional recovery of the acute somatomotor reflexes post Traumatic Brain Injury, took less time to remove adhesive from the forelimbs, and showed higher percentages of correct avoidance responses. CONCLUSION: Our findings indicate that early postTraumatic administration of carbamylated erythropoietin reduces Brain edema development until at least 6 hrs postInjury and improves neurologic recovery. Carbamylated erythropoietin can thus be considered as a potential agent in the treatment of Traumatic Brain Injury-induced diffuse edema.

Geoffrey T Manley - One of the best experts on this subject based on the ideXlab platform.

  • cerebral blood vessel damage in Traumatic Brain Injury
    Clinical Biomechanics, 2018
    Co-Authors: Kenneth L Monson, Matthew I Converse, Geoffrey T Manley
    Abstract:

    Abstract Traumatic Brain Injury is a devastating cause of death and disability. Although Injury of Brain tissue is of primary interest in head trauma, nearly all significant cases include damage of the cerebral blood vessels. Because vessels are critical to the maintenance of the healthy Brain, any Injury or dysfunction of the vasculature puts neural tissue at risk. It is well known that these vessels commonly tear and bleed as an immediate consequence of Traumatic Brain Injury. It follows that other vessels experience deformations that are significant though not severe enough to produce bleeding. Recent data show that such subfailure deformations damage the microstructure of the cerebral vessels, altering both their structure and function. Little is known about the prognosis of these injured vessels and their potential contribution to disease development. The objective of this review is to describe the current state of knowledge on the mechanics of cerebral vessels during head trauma and how they respond to the applied loads. Further research on these topics will clarify the role of blood vessels in the progression of Traumatic Brain Injury and is expected to provide insight into improved strategies for treatment of the disease.

  • cerebral edema in Traumatic Brain Injury pathophysiology and prospective therapeutic targets
    Neurosurgery Clinics of North America, 2016
    Co-Authors: Geoffrey T Manley, Ethan A Winkler, Daniel J Minter
    Abstract:

    : Traumatic Brain Injury is a heterogeneous disorder resulting from an external force applied to the head. The development of cerebral edema plays a central role in the evolution of Injury following Brain trauma and is closely associated with neurologic outcomes. Recent advances in the understanding of the molecular and cellular pathways contributing to the postTraumatic development of cerebral edema have led to the identification of multiple prospective therapeutic targets. The authors summarize the pathogenic mechanisms underlying cerebral edema and highlight the molecular pathways that may be therapeutically targeted to mitigate cerebral edema and associated sequelae following Traumatic Brain Injury.