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 Traumatic brain injury: clinical and pathological parameters in an experimental weightdrop model

2011 ◽  
Vol 26 (2) ◽  
pp. 94-100 ◽  
Author(s):  
Danilo dos Santos Silva ◽  
José Nazareno Pearce de Oliveira Brito ◽  
Jerúsia Oliveira Ibiapina ◽  
Marcel Fernando Miranda Batista Lima ◽  
Andréa Ribeiro Gonçalves de Vasconcelos Medeiros ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Low Cost ◽  
Male Rats ◽  
Group 4 ◽  
Closed Head ◽  
Weight Drop ◽  
Pathologic Analysis ◽  
Trauma Model ◽  
The Impact

PURPOSE: To investigate the function of an experimental cranium trauma model in rats. METHODS: The equipment, already described in the literature and under discreet adaptations, is composed by a platform that produces closed head impact controlled by weight drop with pre-defined and known energy. 25 Wistar male rats (Rattus norvegicus albinus) were divided into five equal groups that received different quantities of cranial impact energy: G1, G2, G3 and G4 with 0,234J, 0,5J, 0,762J and 1J respectively and G5 (Sham). Under intense analgesia, each group was evaluated clinically in a sequence of intervals and had their encephalon removed for pathologic analysis. RESULTS: Important clinical alterations (convulsions, bradycardia, bradypnea and abnormal postures) and focal pathologic (hematomas and hemorrhages) kept proportion with the intensity of the impact. No fracture was observed and the group 4 had 80% mortality rate. CONCLUSION: The experimental cranium trauma animal model by weight drop is an alternative of low cost and easy reproduction that allows evaluating clinical and pathological alterations in accordance with studies in experimental surgery aims for new traumatic brain injury approach in rats.

scholarly journals Cerebrovascular reactivity in patients with cerebral contusion and its possible pharmacological correction

2016 ◽  
Vol 97 (6) ◽  
pp. 903-908
Author(s):  
R F Garifullin ◽  
V I Danilov ◽  
R H Karimov
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Brain Injury ◽  
Cerebrovascular Reactivity ◽  
Comprehensive Treatment ◽  
Cerebral Contusion ◽  
Comprehensive Therapy ◽  
Acute Traumatic Brain Injury ◽  
Group 2 ◽  
Group 1

Aim. Evaluation of dimephosphone as a medication for correction of cerebrovascular reactivity damage in patients with acute traumatic brain injury of mild to moderate severity.Methods. The study included 40 patients with acute traumatic brain injury admitted to the Department of Neurosurgery of Kazan City Clinical Hospital №7. All patients were divided into 2 groups: patients who did not receive dimephosphone were included in group 1, in group 2 patients received drug therapy identical to that in group 1 but with additional 15% solution of dimephosphone 15 ml 3 times a day for 12 days. Evaluation of cerebral blood flow was conducted by transcranial Doppler with the use of analyzer of blood flow velocity «Sonomed 300M». Patients underwent daily functional tests (compression test, hypercapnic test, hypocapnic test) during the days 1 to 12 of hospital stay.Results. The conducted study confirms disorders of cerebrovascular reactivity in patients with acute traumatic brain injury. Also it was found that patients treated with dimephosphone as part of comprehensive therapy at a dose of 15 ml of 15% solution 3 times a day, cerebrovascular reactivity indices (index of vasomotor reactivity, overshoot coefficient) recovered significantly faster.Conclusion. All patients in the acute period of traumatic brain injury with cerebral contusion have disorders of cerebrovascular reactivity; recovery of cerebrovascular reactivity in patients with traumatic brain injury is accelerated by inclusion of dimephosphone in comprehensive treatment.

Regional cerebrovascular responses to progressive hypotension after traumatic brain injury in cats

1992 ◽  
Vol 263 (4) ◽  
pp. H1276-H1284 ◽  
Author(s):  
D. S. DeWitt ◽  
D. S. Prough ◽  
C. L. Taylor ◽  
J. M. Whitley ◽  
D. D. Deal ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Regions ◽  
Group Iv ◽  
Group Iii ◽  
Hemorrhagic Hypotension ◽  
Isoflurane Anesthesia ◽  
Group I ◽  
Injury Group ◽  
Group Ii

We investigated the effects of hypotension on cerebral blood flow (CBF) after traumatic brain injury (TBI) in cats. Isoflurane-anesthetized cats were prepared for TBI and for microsphere measurements of total (T) and regional (r) CBF. Four groups were studied: sham injury (group I, n = 6); TBI (group II, n = 6); isoflurane anesthesia, no TBI or hypotension (group III, n = 4); and isoflurane and TBI, no hypotension (group IV, n = 8). After TBI or sham trauma, mean arterial pressure (MAP) was reduced to 80, 60, and 40 mmHg by hemorrhage. Group I TCBF did not change significantly from baseline until MAP reached 40 mmHg, but rCBF was more dependent on MAP in anterior hemispheric than in brain stem regions. Group II TCBF was significantly lower than baseline, and group I TCBF at all levels of hypotension and autoregulation was impaired at higher MAP levels in anterior than in posterior brain regions. Groups III and IV indicated that decreases in TCBF were not due to duration of the preparation or to TBI in the absence of hemorrhagic hypotension. We conclude that global and regional autoregulation are absent in response to hemorrhagic hypotension after TBI.

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.

Artifact removal from neurophysiological signals: impact on intracranial and arterial pressure monitoring in traumatic brain injury

2020 ◽  
Vol 132 (6) ◽  
pp. 1952-1960 ◽  
Author(s):  
Seung-Bo Lee ◽  
Hakseung Kim ◽  
Young-Tak Kim ◽  
Frederick A. Zeiler ◽  
Peter Smielewski ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Status ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Clinical Parameters ◽  
Artifact Removal ◽  
Clinical Events ◽  
Arterial Blood ◽  
Before And After

OBJECTIVEMonitoring intracranial and arterial blood pressure (ICP and ABP, respectively) provides crucial information regarding the neurological status of patients with traumatic brain injury (TBI). However, these signals are often heavily affected by artifacts, which may significantly reduce the reliability of the clinical determinations derived from the signals. The goal of this work was to eliminate signal artifacts from continuous ICP and ABP monitoring via deep learning techniques and to assess the changes in the prognostic capacities of clinical parameters after artifact elimination.METHODSThe first 24 hours of monitoring ICP and ABP in a total of 309 patients with TBI was retrospectively analyzed. An artifact elimination model for ICP and ABP was constructed via a stacked convolutional autoencoder (SCAE) and convolutional neural network (CNN) with 10-fold cross-validation tests. The prevalence and prognostic capacity of ICP- and ABP-related clinical events were compared before and after artifact elimination.RESULTSThe proposed SCAE-CNN model exhibited reliable accuracy in eliminating ABP and ICP artifacts (net prediction rates of 97% and 94%, respectively). The prevalence of ICP- and ABP-related clinical events (i.e., systemic hypotension, intracranial hypertension, cerebral hypoperfusion, and poor cerebrovascular reactivity) all decreased significantly after artifact removal.CONCLUSIONSThe SCAE-CNN model can be reliably used to eliminate artifacts, which significantly improves the reliability and efficacy of ICP- and ABP-derived clinical parameters for prognostic determinations after TBI.

scholarly journals Enriching neural stem cell and anti‐inflammatory glial phenotypes with electrical stimulation after traumatic brain injury in male rats

2021 ◽  
Author(s):  
Eunyoung Park ◽  
Johnathan G. Lyon ◽  
Melissa Alvarado‐Velez ◽  
Martha I. Betancur ◽  
Nassir Mokarram ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cell ◽  
Electrical Stimulation ◽  
Brain Injury ◽  
Neural Stem Cell ◽  
Male Rats ◽  
Anti Inflammatory

scholarly journals Serum S100B Determination in the Management of Pediatric Mild Traumatic Brain Injury

2012 ◽  
Vol 58 (7) ◽  
pp. 1116-1122 ◽  
Author(s):  
Damien Bouvier ◽  
Mathilde Fournier ◽  
Jean-Benoît Dauphin ◽  
Flore Amat ◽  
Sylvie Ughetto ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Reference Interval ◽  
Pediatric Emergency ◽  
Cranial Computed Tomography ◽  
Serum S100b ◽  
Significant Difference ◽  
Hospitalization Costs ◽  
Group 2

Abstract BACKGROUND The place of serum S100B measurement in mild traumatic brain injury (mTBI) management is still controversial. Our prospective study aimed to evaluate its utility in the largest child cohort described to date. METHODS Children younger than 16 years presenting at a pediatric emergency department within 3 h after TBI were enrolled prospectively for blood sampling to determine serum S100B concentrations. The following information was collected: TBI severity determined by using the Masters classification [1: minimal or Glasgow Coma Scale (GCS) 15, 2: mild or GCS 13–15, and 3: severe or GCS &lt;13]; whether hospitalized or not; good or bad clinical evolution (CE); whether cranial computed tomography (CCT) was prescribed; and related presence (CCT+) or absence (CCT−) of lesions. RESULTS For the 446 children enrolled, the median concentrations of S100B were 0.21, 0.31, and 0.44 μg/L in Masters groups 1, 2, and 3, respectively, with a statistically significant difference between these groups (P &lt; 0.05). In Masters group 2, 65 CCT scans were carried out. Measurement of S100B identified patients as CCT+ with 100% (95% CI 85–100) sensitivity and 33% (95% CI 20–50) specificity. Of the 424 children scored Masters 1 or 2, 21 presented “bad CE.” S100B identified bad CE patients with 100% (95% CI 84–100) sensitivity and 36% (95% CI 31–41) specificity. Of the 242 children hospitalized, 81 presented an S100B concentration within the reference interval. CONCLUSIONS Serum S100B determination during the first 3 h of management of children with mTBI has the potential to reduce the number of CCT scans, thereby avoiding unnecessary irradiation, and to save hospitalization costs.

scholarly journals Inhaled Nitric Oxide Reduces Secondary Brain Damage after Traumatic Brain Injury in Mice

2012 ◽  
Vol 33 (2) ◽  
pp. 311-318 ◽  
Author(s):  
Nicole A Terpolilli ◽  
Seong-Woong Kim ◽  
Serge C Thal ◽  
Wolfgang M Kuebler ◽  
Nikolaus Plesnila
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Brain Regions ◽  
Lesion Volume ◽  
Effective Treatment Option ◽  
Secondary Brain Damage ◽  
Edema Formation ◽  
Regional Ischemia

Ischemia, especially pericontusional ischemia, is one of the leading causes of secondary brain damage after traumatic brain injury (TBI). So far efforts to improve cerebral blood flow (CBF) after TBI were not successful because of various reasons. We previously showed that nitric oxide (NO) applied by inhalation after experimental ischemic stroke is transported to the brain and induces vasodilatation in hypoxic brain regions, thus improving regional ischemia, thereby improving brain damage and neurological outcome. As regional ischemia in the traumatic penumbra is a key mechanism determining secondary posttraumatic brain damage, the aim of the current study was to evaluate the effect of NO inhalation after experimental TBI. NO inhalation significantly improved CBF and reduced intracranial pressure after TBI in male C57 Bl/6 mice. Long-term application (24 hours NO inhalation) resulted in reduced lesion volume, reduced brain edema formation and less blood–brain barrier disruption, as well as improved neurological function. No adverse effects, e.g., on cerebral auto-regulation, systemic blood pressure, or oxidative damage were observed. NO inhalation might therefore be a safe and effective treatment option for TBI patients.

Sign in / Sign up

Export Citation Format

Share Document