Search results for "Traumatic Brain Injury"

showing 10 items of 121 documents

An early bolus of hypertonic saline hydroxyethyl starch improves long-term outcome after global cerebral ischemia.

2006

Objective: The beneficial effect of hypertonic saline solutions in the emergency treatment of shock and traumatic brain injury is well described. The present study determines effects of a single bolus of hypertonic saline on long-term survival, neurologic function, and neuronal survival 10 days after global cerebral ischemia. In addition, we evaluated the therapeutic window for hypertonic saline treatment (early vs. delayed application). Design: Laboratory experiment. Setting: University laboratory. Subjects: Male Wistar rats weighing 240‐330 g. Interventions: Rats were submitted to temporal global cerebral ischemia using temporary bilateral carotid occlusion combined with hypobaric hypoten…

MaleTime FactorsTraumatic brain injurymedicine.medical_treatmentIschemiaPlasma SubstitutesBlood PressureHydroxyethyl starchCritical Care and Intensive Care MedicineWeight GainBrain IschemiaHydroxyethyl Starch DerivativesBolus (medicine)Intensive caremedicineAnimalsRats WistarSalineNeuronsSaline Solution HypertonicCell Deathbusiness.industrySodiumBrainmedicine.diseaseHypertonic salineRatsCerebral blood flowHematocritAnesthesiaReperfusionPotassiumbusinessmedicine.drugCritical care medicine
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2-Methoxyestradiol confers neuroprotection and inhibits a maladaptive HIF-1α response after traumatic brain injury in mice

2014

HIF-1α is pivotal for cellular homeostasis in response to cerebral ischemia. Pharmacological inhibition of HIF-1α may reduce secondary brain damage by targeting post-translational mechanisms associated with its proteasomal degradation and nuclear translocation. This study examined the neuroprotective effects of 2-methoxyestradiol (2ME2), the involved HIF-1α-dependent response, and alternative splicing in exon 14 of HIF-1α (HIF-1α∆Ex14) after traumatic brain injury (TBI) in mice. Intraperitoneal 2ME2 administration 30 min after TBI caused a dose-dependent reduction in secondary brain damage after 24 h. 2ME2 was physiologically tolerated, showed no effects on immune cell brain migration, and …

MaleTraumatic brain injuryBlotting WesternIschemiaCellular homeostasisBrain damagePharmacologyBiologyBiochemistryNeuroprotectionBrain IschemiaMitochondrial ProteinsMiceCellular and Molecular Neurosciencechemistry.chemical_compoundPlasminogen Activator Inhibitor 1medicineAnimalsCell NucleusNeuronsEstradiolTumor Necrosis Factor-alphaAlternative splicingMembrane ProteinsExonsHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseImmunohistochemistryUp-RegulationMice Inbred C57BLAlternative SplicingProtein TransportNeuroprotective AgentsGene Expression RegulationchemistryBrain InjuriesPlasminogen activator inhibitor-1Tumor necrosis factor alphamedicine.symptomNeuroscienceInjections IntraperitonealSubcellular FractionsJournal of Neurochemistry
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The antioxidative, non-psychoactive tricyclic phenothiazine reduces brain damage after experimental traumatic brain injury in mice.

2014

Abstract Oxidative stress due to free radical formation is an important mechanism of secondary brain damage following traumatic brain injury (TBI). Phenothiazine has been found to be a strong antioxidant in eukaryotic cells in vitro and in invertebrates in vivo. The present study was designed to determine the neuroprotective potency of unsubstituted phenothiazine in a paradigm of acute brain injury. Thirty minutes after pneumatic, controlled cortical impact (CCI) injury, C57BI6 mice were randomly assigned to “low dose” (3 mg/kg, LD) or “high dose” (30 mg/kg, HD) s.c. phenothiazine or vehicle treatment. Brain lesion, neurofunctional impairment, body weight, and markers of cerebral inflammati…

MaleTraumatic brain injuryGene ExpressionInflammationCell CountBrain damagePharmacologymedicine.disease_causeNeuroprotectionAntioxidantsRandom AllocationIn vivoPhenothiazinesMedicineAnimalschemistry.chemical_classificationInflammationDose-Response Relationship Drugbusiness.industryGeneral NeuroscienceCalcium-Binding ProteinsMicrofilament ProteinsBrainmedicine.diseaseMice Inbred C57BLchemistryAnesthesiaBrain InjuriesTumor necrosis factor alphamedicine.symptombusinessNeurogliaOxidative stressTricyclicNeuroscience letters
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Propofol Impairs Neurogenesis and Neurologic Recovery and Increases Mortality Rate in Adult Rats After Traumatic Brain Injury*

2013

Objective: Limited data are available on the influence of sedation for critical care therapy with the widely used anesthetic propofol on recovery from acute traumatic brain injury. To establish the influence of propofol on endogenous neurogenesis and functional recovery after traumatic brain injury, rats were sedated with propofol either during or 2 hours after experimental traumatic brain injury. Design: Randomized controlled animal study. Setting: University research laboratory. Subjects: One hundred sixteen male Sprague Dawley rats. Interventions: Mechanical brain lesion by controlled cortical impact. Measurements and Main Results: This study investigated the dose-dependent influence of …

MaleTraumatic brain injuryNeurogenesisSedationCritical Care and Intensive Care MedicineSevofluraneRats Sprague-DawleyCognitionAnimalsHypnotics and SedativesMedicineMaze LearningPropofolDose-Response Relationship Drugbusiness.industryMortality rateNeurogenesisBrainRecovery of Functionmedicine.diseaseRatsDose–response relationshipBrain InjuriesAnesthesiaAnestheticmedicine.symptombusinessPropofolmedicine.drugCritical Care Medicine
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Xenon Improves Neurologic Outcome and Reduces Secondary Injury Following Trauma in an In Vivo Model of Traumatic Brain Injury*

2014

Objectives: To determine the neuroprotective efficacy of the inert gas xenon following traumatic brain injury and to determine whether application of xenon has a clinically relevant therapeutic time window. Design: Controlled animal study. Setting: University research laboratory. Subjects: Male C57BL/6N mice (n = 196). Interventions: Seventy-five percent xenon, 50% xenon, or 30% xenon, with 25% oxygen (balance nitrogen) treatment following mechanical brain lesion by controlled cortical impact. Measurements and Main Results: Outcome following trauma was measured using 1) functional neurologic outcome score, 2) histological measurement of contusion volume, and 3) analysis of locomotor functio…

MaleXenonINTRACRANIAL-PRESSURE1110 NursingCritical Care and Intensive Care MedicineGAIT ABNORMALITIESXenonGaitIntracranial pressureintegumentary systemBrainGLYCINE SITEINTRACEREBRAL-HEMORRHAGED-ASPARTATE RECEPTORNeuroprotective AgentsTreatment OutcomeAnesthesiahead traumaneuroprotectionLife Sciences & BiomedicinePOTASSIUM CHANNELSLocomotioncirculatory and respiratory physiologyinorganic chemicalsTraumatic brain injurychemistry.chemical_elementNeuroprotection1117 Public Health and Health ServicesHead traumaCritical Care MedicineIn vivoGeneral & Internal MedicineAdministration InhalationmedicineAnimalscardiovascular diseasesIntracerebral hemorrhageScience & Technologybusiness.industry1103 Clinical Sciencesbrain injurymedicine.diseaseCONTROLLED CORTICAL IMPACTCOMPETITIVE-INHIBITIONEmergency & Critical Care MedicineMice Inbred C57BLDisease Models AnimalCOGNITIVE DEFICITSchemistryBrain InjuriesClosed head injurybusinessCLOSED-HEAD INJURYinert gasesCritical Care Medicine
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Xenon improves long-term cognitive function, reduces neuronal loss and chronic neuroinflammation, and improves survival after traumatic brain injury …

2019

Background.Xenon is a noble gas with neuroprotective properties. We previously showed that xenon improves short and long-term outcomes in young adult mice after controlled cortical impact (CCI). This is a follow-up study investigating xenon’s effect on very long-term outcome and survival. Methods.C57BL/6N (n=72) young adult male mice received single CCI or sham surgery and were treated with either xenon (75%Xe:25%O2) or control gas (75% N2:25%O2). The outcomes used were: 1) 24-hour lesion volume and neurological outcome score; 2)contextual fear-conditioning at 2 weeks and 20 months; 3) corpus callosum white matter quantification; 4) immunohistological assessment of neuroinflammation and neu…

MaleXenonhippocampusnerve degenerationCorpus callosumBUPRENORPHINEneuroinflammationMice0302 clinical medicineCognition030202 anesthesiologyAnesthesiologyBrain Injuries TraumaticMedicineEPIDEMIOLOGYYoung adultmemory disordersNeuronstraumatic brain injurySham surgeryBrain3. Good healthD-ASPARTATE RECEPTORmedicine.anatomical_structureNeuroprotective AgentsAnesthesianeuroprotectionmedicine.symptomLife Sciences & BiomedicineTraumatic brain injuryHYPOPITUITARISMNeuroprotectionWhite matter03 medical and health sciencesANALGESIAINHALED XENONAnimalsgeneral anaesthesiaSurvival analysisHYPOTHERMIAInflammationScience & Technologybusiness.industry1103 Clinical SciencesHypothermiamedicine.diseaseCOMPETITIVE-INHIBITIONSurvival AnalysisMice Inbred C57BLPATHOLOGYDisease Models AnimalAnesthesiology and Pain MedicineChronic DiseasebusinessCognition Disorders030217 neurology & neurosurgeryWHITE-MATTER DAMAGEFollow-Up StudiesBritish journal of anaesthesia
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Hypertonic saline solution and decompressive craniectomy for treatment of intracranial hypertension in pediatric severe traumatic brain injury.

2002

Experimental data 8 –11 and first clinical results in adults 12,13 suggest that hypertonic saline ( 1.0) may be highly effective in lowering ICP even when mannitol has lost its therapeutic potential after prolonged and repeated use. In children, only limited experience exists with the use of hypertonic saline solutions: a randomized prospective study in children with severe head injury compared the effects on ICP (increased to 15–20 mm Hg) of isotonic (0.9% NaCl) and hypertonic (3% NaCl) saline injections, demonstrating a beneficial effect of the hypertonic solution. 14 Another prospective randomized trial compared the effects of continuous infusion of either lactated Ringer’s solution (277…

Malemedicine.medical_specialtyIntracranial PressureTraumatic brain injurymedicine.medical_treatmentBrain damageCritical Care and Intensive Care MedicineDrug Administration ScheduleInjury Severity ScorePreoperative CaremedicineHumansChildInfusions IntravenousSalineOsmolePostoperative CareSaline Solution Hypertonicbusiness.industryHead injurySodiumGlasgow Coma ScaleAccidents Trafficmedicine.diseaseDecompression SurgicalHypertonic salineSurgeryAnesthesiaBrain InjuriesSurgeryDecompressive craniectomyAccidental Fallsmedicine.symptomIntracranial HypertensionbusinessTomography X-Ray ComputedCraniotomyThe Journal of trauma
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LACTATE, NOT GLUCOSE, UP-REGULATES MITOCHONDRIAL OXYGEN CONSUMPTION BOTHIN SHAM AND LATERAL FLUID PERCUSSED RAT BRAINS

2006

OBJECTIVE: Failure of energy metabolism after traumatic brain injury may be a major factor limiting outcome. Although glucose is the primary metabolic substrate in the healthy brain, the well documented surge in tissue lactate after traumatic brain injury suggests that lactate may provide an energy need that cannot be met by glucose. We hypothesized, therefore, that administration of lactate or the combination of lactate and supraphysiological oxygen may improve mitochondrial oxidative respiration in the brain after rat fluid percussion injury. We measured oxygen consumption (VO2) to determine what effects glucose, lactate, oxygen, and the combination of lactate and oxygen have on mitochond…

Malemedicine.medical_specialtyTraumatic brain injuryCell RespirationOxidative phosphorylationMitochondrionRats Sprague-Dawleychemistry.chemical_compoundOxygen ConsumptionFraction of inspired oxygenInternal medicineRespirationmedicineAnimalsLactic AcidDose-Response Relationship Drugbusiness.industryBrainmedicine.diseaseMitochondriaRatsUp-RegulationCartesian diverLactic acidOxygenDose–response relationshipGlucoseEndocrinologychemistryBrain InjuriesAnesthesiaSurgeryNeurology (clinical)businessNeurosurgery
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The relation between the incidence of hypernatremia and mortality in patients with severe traumatic brain injury

2009

Introduction The study was aimed at verifying whether the occurrence of hypernatremia during the intensive care unit (ICU) stay increases the risk of death in patients with severe traumatic brain injury (TBI). We performed a retrospective study on a prospectively collected database including all patients consecutively admitted over a 3-year period with a diagnosis of TBI (post-resuscitation Glasgow Coma Score ≤ 8) to a general/neurotrauma ICU of a university hospital, providing critical care services in a catchment area of about 1,200,000 inhabitants. Methods Demographic, clinical, and ICU laboratory data were prospectively collected; serum sodium was assessed an average of three times per …

Malemedicine.medical_specialtyTraumatic brain injuryCritical Care and Intensive Care MedicineSeverity of Illness Indexlaw.inventionHospitals UniversitylawSeverity of illnessmedicineHumansDeamino Arginine VasopressinIntensive care medicineProportional Hazards ModelsRetrospective StudiesSaline Solution HypertonicHypernatremiabusiness.industryIncidenceResearchIncidence (epidemiology)Glasgow Coma ScaleRetrospective cohort studyMiddle Agedmedicine.diseaseIntensive care unitHypertonic salineIntensive Care UnitsBrain InjuriesEmergency medicineCommentaryFemaleHypernatremiaIntracranial HypertensionbusinessCritical Care
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Pioglitazone Reduces Secondary Brain Damage after Experimental Brain Trauma by PPAR-γ-Independent Mechanisms

2011

Inflammatory and ischemic processes contribute to the development of secondary brain damage after mechanical brain injury. Recent data suggest that thiazolidinediones (TZDs), a class of drugs approved for the treatment of non-insulin-dependent diabetes mellitus, effectively reduces inflammation and brain lesion by stimulation of the peroxisome proliferator-activated receptor-γ (PPAR-γ). The present study investigates the influence of the TZD pioglitazone and rosiglitazone on inflammation and secondary brain damage after experimental traumatic brain injury (TBI). A controlled cortical impact (CCI) injury was induced in male C57BL/6 mice to investigate following endpoints: (1) mRNA expression…

Malemedicine.medical_specialtyTraumatic brain injuryPeroxisome proliferator-activated receptorInflammationStimulationBrain damageMiceDiabetes mellitusInternal medicinemedicineAnimalsHypoglycemic Agentschemistry.chemical_classificationPioglitazonebusiness.industrymedicine.diseaseMice Inbred C57BLPPAR gammaDisease Models AnimalNeuroprotective AgentsEndocrinologychemistryBrain InjuriesBrain Damage ChronicThiazolidinedionesNeurology (clinical)medicine.symptombusinessRosiglitazonePioglitazonemedicine.drugJournal of Neurotrauma
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