scholarly journals Changes in Neuropeptide Y after Experimental Traumatic Brain Injury in the Rat

1992 ◽  
Vol 12 (4) ◽  
pp. 697-702 ◽  
Author(s):  
Tracy K. McIntosh ◽  
Donna Ferriero
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuropeptide Y ◽  
Parietal Cortex ◽  
Brain Regions ◽  
Male Rats ◽  
Post Injury ◽  
Regional Brain ◽  
Left Parietal Cortex ◽  
Experimental Traumatic Brain Injury

We utilized a model of fluid percussion (FP) brain injury in the rat to examine the hypothesis that alterations in brain neuropeptide Y (NPY) concentrations occur following brain injury. Male rats (n = 44) were subjected to FP traumatic brain injury. One group of animals (n = 38) was killed at 1 min, 15 min, 1 h, or 24 h after brain injury, and regional brain homogenates were analyzed for NPY concentrations using radioimmunoassay. A second group of animals (n = 6) was killed for NPY immunocytochemistry. Concentrations of NPY in the injured left parietal cortex were significantly elevated at 15 min post injury (p < 0.05). No changes were observed in other brain regions. NPY-immunoreactive fibers were seen at 15 min post injury predominantly in the injured cortex and adjacent hippocampus. These temporal changes in NPY immunoreactivity, together with previous observations concerning posttraumatic changes in regional CBF in these same areas, suggest that an increase in region NPY concentrations after brain injury may be involved in part in the pathogenesis of posttraumatic hypoperfusion.

scholarly journals Effects of Traumatic Brain Injury on Regional Cerebral Blood Flow in Rats as Measured with Radiolabeled Microspheres

1989 ◽  
Vol 9 (1) ◽  
pp. 117-124 ◽  
Author(s):  
Iwao Yamakami ◽  
Tracy K. McIntosh
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Regions ◽  
Post Injury ◽  
Fluid Percussion ◽  
Hemodynamic Variables ◽  
Acute Changes ◽  
Injury Recovery ◽  
Left Parietal Cortex ◽  
Experimental Traumatic Brain Injury

To clarify the effect of experimental brain injury on regional CBF (rCBF), repeated rCBF measurements were performed using radiolabeled microspheres in rats Subjected to fluid-percussion traumatic brain injury. Three consecutive microsphere injections in six uninjured control rats substantiated that the procedure induces no significant changes in hemodynamic variables or rCBF. Animals were subjected to left parietal fluid-percussion brain injury of moderate severity (2.1–2.4 atm) and rCBF values were determined (a) prior to injury and 15 min and 1 h following injury (n = 7); and (b) prior to injury and 30 min and 2 h following injury (n = 7). At 15 min post injury, there was a profound reduction of rCBF in all brain regions studied (p < 0.01). Although rCBF in the hindbrain had recovered to near-normal by 30 min post injury, rCBF in both injured and contralateral (uninjured) forebrain areas remained significantly suppressed up to 1 h post injury. At 2 h post injury, recovery of rCBF to near-normal values was observed in all brain regions except the focal area of injury (left parietal cortex) where rCBF remained significantly depressed (p < 0.01). This prolonged focal oligemia at the injury site was associated with the development of reproducible cystic necrosis in the left parietotemporal cortex at 4 weeks post injury. Our results demonstrate that acute changes in rCBF occur following experimental traumatic brain injury in rats and that rCBF remains significantly depressed up to 2 h post injury in the area circumscribing the trauma site.

scholarly journals Alterations in Regional Cerebral Blood Flow following Brain Injury in the Rat

1991 ◽  
Vol 11 (4) ◽  
pp. 655-660 ◽  
Author(s):  
Iwao Yamakami ◽  
Tracy K. McIntosh
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Regional Cerebral Blood Flow ◽  
Brain Regions ◽  
Regional Cerebral Blood ◽  
Microsphere Method ◽  
Left Parietal Cortex ◽  
Experimental Traumatic Brain Injury

To elucidate the temporal changes in regional cerebral blood flow (rCBF) after experimental traumatic brain injury, serial rCBF measurements were made during a 24-h period following fluid-percussion (F-P) traumatic brain injury in the rat. Brain injury of 2.2 atm was induced over the left parietal cortex and serial measurements of rCBF were performed using the radiolabeled microsphere method. rCBF values were obtained prior to injury and at 15 and 30 min and 1, 2, 4, and 24 h postinjury. At 15 min postinjury, there was a profound, widespread reduction in rCBF in all brain regions studied (p < 0.05). At 30 min and 1 h postinjury, all brain regions except pons-medulla and cerebellum showed significantly reduced rCBF compared to the preinjury values (p < 0.05). By 2 h postinjury, however, a significant focal reduction of rCBF was observed only in the cerebral tissue surrounding the trauma site (p < 0.05); rCBF in the remaining brain regions had recovered to the preinjury levels. By 4 h postinjury, rCBF had returned to normal in all brain regions studied. This recovery of rCBF was still evident at 24 h postinjury. The present study demonstrates that, following the experimental traumatic brain injury in the rat, (a) an initial global suppression of rCBF occurs up to 1 h postinjury; (b) at the trauma site, a more persistent focal reduction of rCBF occurs; and (c) these alterations in rCBF after trauma dissolve by 4 h postinjury. The result was discussed in the context of the neurological, electroencephalographic, magnetic resonance spectroscopic, and pathological findings observed in our lateral F-P brain injury rat model.

Outcome measures from experimental traumatic brain injury in male rats vary with the complete temporal biomechanical profile of the injury event

2020 ◽  
Vol 98 (10) ◽  
pp. 2027-2044
Author(s):  
Radia Abdul‐Wahab ◽  
Mathew T. Long ◽  
Rafael Ordaz ◽  
Bruce G. Lyeth ◽  
Bryan J. Pfister
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Outcome Measures ◽  
Male Rats ◽  
Injury Event ◽  
Experimental Traumatic Brain Injury

scholarly journals Administration of a 20-Hydroxyeicosatetraenoic Acid Synthesis Inhibitor Improves Outcome in a Rat Model of Pediatric Traumatic Brain Injury

2019 ◽  
Vol 41 (3-4) ◽  
pp. 166-176 ◽  
Author(s):  
Shiyu Shu ◽  
Zhi Zhang ◽  
Dawn Spicer ◽  
Ewa Kulikowicz ◽  
Ke Hu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Ischemia Reperfusion ◽  
Memory Task ◽  
Male Rats ◽  
Lesion Volume ◽  
Hydroxyeicosatetraenoic Acid ◽  
Post Injury ◽  
Synthesis Inhibitor ◽  
Tnf Α

The arachidonic acid pathway metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) contributes to ischemia/reperfusion brain injury. Inhibition of 20-HETE formation can protect the developing brain from global ischemia. Here, we examined whether treatment with the 20-HETE synthesis inhibitor N-hydroxy-N-4-butyl-2-methylphenylformamidine (HET0016) can protect the immature brain from traumatic brain injury (TBI). Male rats at postnatal day 9–10 underwent controlled cortical impact followed by intraperitoneal injection with vehicle or HET0016 (1 mg/kg, 5 min and 3 h post-injury). HET0016 decreased the lesion volume by over 50% at 3 days of recovery, and this effect persisted at 30 days as the brain matured. HET0016 decreased peri-lesion gene expression of proinflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin-1β [IL-1β]) at 1 day and increased reparative cytokine (IL-4, IL-10) expression at 3 days. It also partially preserved microglial ramified processes, consistent with less activation. HET0016 decreased contralateral hindlimb foot faults and improved outcome on the novel object recognition memory task 30 days after TBI. In cultured BV2 microglia, HET0016 attenuated the lipopolysaccharide-evoked increase in release of TNF-α. Our data show that HET0016 improves acute and long-term histologic and functional outcomes, in association with an attenuated neuroinflammatory response after contusion of an immature rat brain.

scholarly journals Delayed Hemorrhagic Hypotension Exacerbates the Hemodynamic and Histopathologic Consequences of Traumatic Brain Injury in Rats

2001 ◽  
Vol 21 (7) ◽  
pp. 847-856 ◽  
Author(s):  
Yoshitaro Matsushita ◽  
Helen M. Bramlett ◽  
John W. Kuluz ◽  
Ofelia Alonso ◽  
W. Dalton Dietrich
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Posterior Parietal Cortex ◽  
Brain Regions ◽  
Cerebrovascular Reactivity ◽  
Male Rats ◽  
Hemorrhagic Hypotension ◽  
Group 4 ◽  
Histopathologic Evaluation ◽  
Group 2

Alterations in cerebral autoregulation and cerebrovascular reactivity after traumatic brain injury (TBI) may increase the susceptibility of the brain to secondary insults, including arterial hypotension. The purpose of this study was to evaluate the consequences of mild hemorrhagic hypotension on hemodynamic and histopathologic outcome after TBI. Intubated, anesthetized male rats were subjected to moderate (1.94 to 2.18 atm) parasagittal fluid–percussion (FP) brain injury. After TBI, animals were exposed to either normotension (group 1: TBI alone, n = 6) or hypotension (group 2: TBI + hypotension, n = 6). Moderate hypotension (60 mm Hg/30 min) was induced 5 minutes after TBI or sham procedures by hemorrhage. Sham-operated controls (group 3, n = 7) underwent an induced hypotensive period, whereas normotensive controls (group 4, n = 4) did not. For measuring regional cerebral blood flow (rCBF), radiolabeled microspheres were injected before, 20 minutes after, and 60 minutes after TBI (n = 23). For quantitative histopathologic evaluation, separate groups of animals were perfusion-fixed 3 days after TBI (n = 22). At 20 minutes after TBI, rCBF was bilaterally reduced by 57% ± 6% and 48% ± 11% in cortical and subcortical brain regions, respectively, under normotensive conditions. Compared with normotensive TBI rats, hemodynamic depression was significantly greater with induced hypotension in the histopathologically vulnerable (P1) posterior parietal cortex ( P < 0.01). Secondary hypotension also increased contusion area at specific bregma levels compared with normotensive TBI rats ( P < 0.05), as well as overall contusion volume (0.96 ± 0.46 mm3 vs. 2.02 ± 0.51 mm3, mean ± SD, P < 0.05). These findings demonstrate that mild hemorrhagic hypotension after FP injury worsens local histopathologic outcome, possibly through vascular mechanisms.

scholarly journals Connectomic Assessment of Injury Burden and Longitudinal Structural Network Alterations in Moderate-to-severe Traumatic Brain Injury

2021 ◽  
Author(s):  
Yusuf Osmanlioglu ◽  
Drew Parker ◽  
Jacob A Alappatt ◽  
James J Gugger ◽  
Ramon R Diaz-Arrastia ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Structural Connectivity ◽  
Public Health Problem ◽  
Brain Regions ◽  
Brain Network ◽  
Major Public Health Problem ◽  
Post Injury ◽  
Structural Network ◽  
Injury Burden

Traumatic brain injury (TBI) is a major public health problem. Caused by external mechanical forces, a major characteristic of TBI is the shearing of axons across the white matter, which causes structural connectivity disruptions between brain regions. This diffuse injury leads to cognitive deficits, frequently requiring rehabilitation. Heterogeneity is another characteristic of TBI as severity and cognitive sequelae of the disease have a wide variation across patients, posing a big challenge for treatment. Thus, measures assessing network-wide structural connectivity disruptions in TBI are necessary to quantify injury burden of individuals, which would help in achieving personalized treatment, patient monitoring, and rehabilitation planning. Despite TBI being a disconnectivity syndrome, connectomic assessment of structural disconnectivity has been very scarce. In this study, we propose a novel connectomic measure that we call network anomaly score (NAS) to capture the integrity of structural connectivity in TBI patients by leveraging two major characteristics of the disease: diffuseness of axonal injury and heterogeneity of the disease. Over a longitudinal cohort of moderate-to-severe TBI patients, we demonstrate that structural network topology of patients are more heterogeneous and are significantly different than that of healthy controls at 3 months post-injury, where dissimilarity further increases up to 12 months. We also show that NAS captures injury burden as quantified by post-traumatic amnesia and that alterations in the structural brain network is not related to cognitive recovery. Finally we compare NAS to major graph theory measures used in TBI literature and demonstrate the superiority of NAS in characterizing the disease.

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.

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