In vivo measurement of tissue damage, oxygen saturation changes and blood flow changes after experimental traumatic brain injury in rats using susceptibility weighted imaging

2007 ◽  
Vol 25 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Yimin Shen ◽  
Zhifeng Kou ◽  
Christian W. Kreipke ◽  
Theodor Petrov ◽  
Jiani Hu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Brain Injury ◽  
Oxygen Saturation ◽  
Tissue Damage ◽  
Susceptibility Weighted Imaging ◽  
In Vivo Measurement ◽  
Flow Changes ◽  
Experimental Traumatic Brain Injury

scholarly journals Traumatic Brain Injury by a Closed Head Injury Device Induces Cerebral Blood Flow Changes and Microhemorrhages

2015 ◽  
Vol 5 ◽  
pp. 52 ◽  
Author(s):  
Srinivasu Kallakuri ◽  
Sharath Bandaru ◽  
Nisrine Zakaria ◽  
Yimin Shen ◽  
Zhifeng Kou ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Head Injury ◽  
Corpus Callosum ◽  
Closed Head Injury ◽  
Susceptibility Weighted Imaging ◽  
Closed Head ◽  
Flow Changes

Objectives: Traumatic brain injury is a poly-pathology characterized by changes in the cerebral blood flow, inflammation, diffuse axonal, cellular, and vascular injuries. However, studies related to understanding the temporal changes in the cerebral blood flow following traumatic brain injury extending to sub-acute periods are limited. In addition, knowledge related to microhemorrhages, such as their detection, localization, and temporal progression, is important in the evaluation of traumatic brain injury. Materials and Methods: Cerebral blood flow changes and microhemorrhages in male Sprague Dawley rats at 4 h, 24 h, 3 days, and 7 days were assessed following a closed head injury induced by the Marmarou impact acceleration device (2 m height, 450 g brass weight). Cerebral blood flow was measured by arterial spin labeling. Microhemorrhages were assessed by susceptibility-weighted imaging and Prussian blue histology. Results: Traumatic brain injury rats showed reduced regional and global cerebral blood flow at 4 h and 7 days post-injury. Injured rats showed hemorrhagic lesions in the cortex, corpus callosum, hippocampus, and brainstem in susceptibility-weighted imaging. Injured rats also showed Prussian blue reaction products in both the white and gray matter regions up to 7 days after the injury. These lesions were observed in various areas of the cortex, corpus callosum, hippocampus, thalamus, and midbrain. Conclusions: These results suggest that changes in cerebral blood flow and hemorrhagic lesions can persist for sub-acute periods after the initial traumatic insult in an animal model. In addition, microhemorrhages otherwise not seen by susceptibility-weighted imaging are present in diverse regions of the brain. The combination of altered cerebral blood flow and microhemorrhages can potentially be a source of secondary injury changes following traumatic brain injury and may need to be taken into consideration in the long-term care of these cases.

scholarly journals Relationship between Flow-Metabolism Uncoupling and Evolving Axonal Injury after Experimental Traumatic Brain Injury

2004 ◽  
Vol 24 (9) ◽  
pp. 1025-1036 ◽  
Author(s):  
Szu-Fu Chen ◽  
Hugh K. Richards ◽  
Piotr Smielewski ◽  
Peter Johnström ◽  
Raymond Salvador ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Brain Injury ◽  
Axonal Injury ◽  
Acute Injury ◽  
Ipsilateral Hemisphere ◽  
Additional Group ◽  
Controlled Cortical Impact Injury ◽  
Impact Injury ◽  
Experimental Traumatic Brain Injury

Blood flow-metabolism uncoupling is a well-documented phenomenon after traumatic brain injury, but little is known about the direct consequences for white matter. The aim of this study was to quantitatively assess the topographic interrelationship between local cerebral blood flow (LCBF) and glucose metabolism (LCMRglc) after controlled cortical impact injury and to determine the degree of correspondence with the evolving axonal injury. LCMRglc and LCBF measurements were obtained at 3 hours in the same rat from 18F-fluorodeoxyglucose and 14C-iodoantipyrine coregistered autoradiographic images, and compared to the density of damaged axonal profiles in adjacent sections and in an additional group at 24 hours using beta-amyloid precursor protein (ß-APP) immunohistochemistry. LCBF was significantly reduced over the ipsilateral hemisphere by 48 ± 15% compared with sham-controls, whereas LCMRglc was unaffected, apart from foci of elevated LCMRglc in the contusion margin. Flow-metabolism was uncoupled, indicated by a significant 2-fold elevation in the LCMRglc/LCBF ratio within most ipsilateral structures. There was a significant increase in ß-APP-stained axons from 3 to 24 hours, which was negatively correlated with LCBF and positively correlated with the LCMRglc/LCBF ratio at 3 hours in the cingulum and corpus callosum. Our study indicates a possible dependence of axonal outcome on flow-metabolism in the acute injury stage.

scholarly journals Temporal and Spatial Profile of Bid Cleavage after Experimental Traumatic Brain Injury

2002 ◽  
Vol 22 (8) ◽  
pp. 951-958 ◽  
Author(s):  
Gerhard Franz ◽  
Ronny Beer ◽  
Denis Intemann ◽  
Stanislaw Krajewski ◽  
John C. Reed ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Regions ◽  
Caspase 8 ◽  
Caspase 9 ◽  
Cell Degeneration ◽  
Similar Time ◽  
Impact Injury ◽  
Experimental Traumatic Brain Injury

Apoptosis plays an essential role in the cascade of CNS cell degeneration after traumatic brain injury. However, the underlying mechanisms are poorly understood. The authors examined the temporal profile and cell subtype distribution of the proapoptotic protein Bid from 6 hours to 7 days after cortical impact injury in the rat. Increased protein levels of tBid were seen in the cortex ipsilateral to the injury site from 6 hours to 3 days after trauma. Immunohistologic examinations revealed expression of tBid in neurons, astrocytes, and oligodendrocytes from 6 hours to 3 days after impact injury, and concurrent assessment of DNA damage using TUNEL identified tBid-immunopositive cells with apoptoticlike morphology in the traumatized cortex. Moreover, Bid cleavage and activation of caspase-8 and caspase-9 occurred at similar time points and in similar brain regions (i.e., cortical layers 2 to 5) after impact injury. In contrast, there was no evidence of caspase-8 or caspase-9 processing or Bid cleavage in the ipsilateral hippocampus, contralateral cortex, and hippocampus up to 7 days after the injury. The results provide the first evidence of Bid cleavage in the traumatized cortex after experimental traumatic brain injury in vivo, and demonstrate that tBid is expressed in neurons and glial cells. Further, findings indicate that cleavage of Bid may be associated with the activation of the initiator caspase-8 and caspase-9. Finally, these data support the hypothesis that cleavage of Bid contributes to the apoptotic degeneration of different CNS cells in the injured cortex.

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.

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