scholarly journals Effect of melatonin on regeneration of cortical neurons in rats with traumatic brain injury

2020 ◽  
Vol 43 (4) ◽  
pp. E8-16
Author(s):  
Jianbin Ge ◽  
Dandan Chen ◽  
Jingjing Ben ◽  
Xinjian Song ◽  
Linqing Zou ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Cognitive Function ◽  
Cortical Neurons ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Vehicle Group ◽  
Post Injury ◽  
Doppler Flowmetry

Purpose: To investigate the effect of melatonin on regeneration of cortical neurons in rats with traumatic brain injury (TBI). Methods: Sprague-Dawley rats (n=36) were randomly divided into sham, TBI+vehicle and TBI+melatonin groups. Cerebral blood flow and cognitive function were observed via laser Doppler flowmetry and by Morris water maze testing, respectively. The serum malondialdehyde (MDA) and superoxide dismutase (SOD) levels were used to assess oxidative stress. Immunofluorescence and terminal deoxynucleotidyl transferase dUTP nick end labelling assay was used to observe the newborn neurons and apoptotic cells. Results: Cerebral blood flow in the TBI+melatonin group was higher than that of the TBI+vehicle group at one, 12, 24 and 48 h post-injury, but the difference was not statistically significant (P>0.05). The cognitive function of the rats was better in the TBI+melatonin group than the TBI+vehicle group (P

Amelioration of hypoperfusion after traumatic brain injury by in vivo endothelin-1 knockout

2009 ◽  
Vol 87 (5) ◽  
pp. 379-386 ◽  
Author(s):  
Theodor Petrov
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Sprague Dawley ◽  
Cross Sectional ◽  
Doppler Flowmetry ◽  
Endothelin 1 ◽  
Time Period

Endothelin 1 (ET-1) is one of the most powerful vasoconstrictors in the brain. Its expression is upregulated after traumatic brain injury (TBI) and is a major factor in the ensuing hypoperfusion. Attenuation of ET-1 effects has been mainly achieved by blockade of its receptors. The result of a direct blockade of ET-1 mRNA synthesis is not known. We used the Marmarou’s model to inflict injury to male Sprague–Dawley rats injected with antisense ET-1 oligodeoxynucleotides (ODNs) before injury. Laser Doppler flowmetry in noninjured rats (2 groups, i.e., untreated and animals that received cODNs) revealed a constant cerebral blood flow of approximately 14 mL·min–1·100 g–1, whereas the values from injured animals pretreated with control ODNs (cODNs) or from animals subjected to TBI alone were approximately 8.0 mL·min–1·100 g–1 during the 18–48 h time period post-TBI. After antisense ET-1 ODNs pretreatment, however, cerebral blood flow in injured animals was approximately 17 mL·min–1·100 g–1 during the 6–48 h time period. Antisense ET-1 ODNs-treated animals also had 19%–29% larger microvessel cross-sectional area and approximately one-third less ET-1 immunoreactivity in the 50–75% range after injury than did cODNs-treated animals after TBI. The results indicate that this direct in vivo approach is an effective therapeutic intervention for the restoration of cerebral blood flow after TBI.

scholarly journals Cerebral Blood Flow after Mild Traumatic Brain Injury: Associations between Symptoms and Post-Injury Perfusion

2018 ◽  
Vol 35 (2) ◽  
pp. 241-248 ◽  
Author(s):  
Jaclyn A. Stephens ◽  
Peiying Liu ◽  
Hanzhang Lu ◽  
Stacy J. Suskauer
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Post Injury

scholarly journals Relationship of Cerebral Blood Flow to Cognitive Function and Recovery in Early Chronic Traumatic Brain Injury

2020 ◽  
Vol 37 (20) ◽  
pp. 2180-2187
Author(s):  
Jeffrey B. Ware ◽  
Sudipto Dolui ◽  
Jeffrey Duda ◽  
Naomi Gaggi ◽  
Robin Choi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Cognitive Function ◽  
Relationship Of

scholarly journals Quantitative cerebral blood flow using xenon-enhanced CT after decompressive craniectomy in traumatic brain injury

2018 ◽  
Vol 129 (1) ◽  
pp. 241-246 ◽  
Author(s):  
Aditya Vedantam ◽  
Claudia S. Robertson ◽  
Shankar P. Gopinath
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Clinical Outcome ◽  
Decompressive Craniectomy ◽  
Decompressive Surgery ◽  
Hemodynamic Parameters ◽  
Enhanced Ct ◽  
The Mean

OBJECTIVEFew studies have reported on changes in quantitative cerebral blood flow (CBF) after decompressive craniectomy and the impact of these measures on clinical outcome. The aim of the present study was to evaluate global and regional CBF patterns in relation to cerebral hemodynamic parameters in patients after decompressive craniectomy for traumatic brain injury (TBI).METHODSThe authors studied clinical and imaging data of patients who underwent xenon-enhanced CT (XeCT) CBF studies after decompressive craniectomy for evacuation of a mass lesion and/or to relieve intractable intracranial hypertension. Cerebral hemodynamic parameters prior to decompressive craniectomy and at the time of the XeCT CBF study were recorded. Global and regional CBF after decompressive craniectomy was measured using XeCT. Regional cortical CBF was measured under the craniectomy defect as well as for each cerebral hemisphere. Associations between CBF, cerebral hemodynamics, and early clinical outcome were assessed.RESULTSTwenty-seven patients were included in this study. The majority of patients (88.9%) had an initial Glasgow Coma Scale score ≤ 8. The median time between injury and decompressive surgery was 9 hours. Primary decompressive surgery (within 24 hours) was performed in the majority of patients (n = 18, 66.7%). Six patients had died by the time of discharge. XeCT CBF studies were performed a median of 51 hours after decompressive surgery. The mean global CBF after decompressive craniectomy was 49.9 ± 21.3 ml/100 g/min. The mean cortical CBF under the craniectomy defect was 46.0 ± 21.7 ml/100 g/min. Patients who were dead at discharge had significantly lower postcraniectomy CBF under the craniectomy defect (30.1 ± 22.9 vs 50.6 ± 19.6 ml/100 g/min; p = 0.039). These patients also had lower global CBF (36.7 ± 23.4 vs 53.7 ± 19.7 ml/100 g/min; p = 0.09), as well as lower CBF for the ipsilateral (33.3 ± 27.2 vs 51.8 ± 19.7 ml/100 g/min; p = 0.07) and contralateral (36.7 ± 19.2 vs 55.2 ± 21.9 ml/100 g/min; p = 0.08) hemispheres, but these differences were not statistically significant. The patients who died also had significantly lower cerebral perfusion pressure (52 ± 17.4 vs 75.3 ± 10.9 mm Hg; p = 0.001).CONCLUSIONSIn the presence of global hypoperfusion, regional cerebral hypoperfusion under the craniectomy defect is associated with early mortality in patients with TBI. Further study is needed to determine the value of incorporating CBF studies into clinical decision making for severe traumatic brain injury.

The Influence of Inhaled Nitric Oxide on Cerebral Blood Flow and Metabolism in a Child with Traumatic Brain Injury

2001 ◽  
Vol 93 (2) ◽  
pp. 351-353 ◽  
Author(s):  
Monica S. Vavilala ◽  
Joan S. Roberts ◽  
Anne E. Moore ◽  
David W. Newell ◽  
Arthur M. Lam
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Inhaled Nitric Oxide

Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Metabolism ◽  
Elevated Intracranial Pressure ◽  
Metabolic Demand ◽  
Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

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