The Effects of Dopamine on Edema Formation in two Models of Traumatic Brain Injury

Beaumont, Andrew; Hayasaki, K.; Marmarou, Anthony; Barzó, Pál; Fatouros, Panos P.; Corwin, Frank

doi:10.1007/978-3-7091-6346-7_30

Cited by 9 publications

(6 citation statements)

References 11 publications

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“…Although a recent study using the CCI model in rats suggests that increased MAP and CPP may exacerbate injury after TBI, in that study, systemic hypertension was induced by large doses of dopamine . Higher doses of dopamine may have produced detrimental effects after injury that were independent of blood pressure (Beaumont et al, 1999). Additionally, our study does not address the important detrimental effect of hypotension following clinical TBI, particularly with multiple trauma.…”

Section: Discussionmentioning

confidence: 93%

Isoflurane Improves Long-Term Neurologic Outcome Versus Fentanyl After Traumatic Brain Injury in Rats

Statler¹,

Kochanek²,

Dixon³

et al. 2000

Journal of Neurotrauma

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Despite routine use of fentanyl in patients after traumatic brain injury (TBI), it is unclear if it is the optimal sedative/analgesic agent. Isoflurane is commonly used in experimental TBI. We hypothesized that isoflurane would be neuroprotective versus fentanyl after TBI. Rats underwent controlled cortical impact (CCI) and received 4 h of N2O/O2 (2:1) and either fentanyl (10 microg/kg i.v. bolus, 50 microg/kg/h infusion) or isoflurane (1% by inhalation) with controlled ventilation. Shams underwent identical preparation, without CCI. Functional outcome (beam balance, beam walking, Morris water maze [MWM] tasks) was assessed over 20 days. Lesion volume and hippocampal neuron survival were quantified on day 21. Additional rats underwent identical CCI and anesthesia with intracranial pressure (ICP) monitoring, and brain water content was assessed. Motor and MWM performances were better in injured rats treated with isoflurane versus fentanyl (p < 0.05). CA1 hippocampal damage was attenuated in isoflurane-treated rats (p < 0.05). Fentanyl-treated rats had higher mean arterial blood pressure after injury (p < 0.05); however, ICP and brain water were similar between groups. Isoflurane improved functional outcome and attenuated damage to CA1 versus fentanyl in rats subjected to CCI. Isoflurane may be neuroprotective by augmenting cerebral blood flow and/or reducing excitotoxicity, not by reducing ICP or brain water content. Alternatively, fentanyl may be detrimental. Isoflurane may mask beneficial effects of novel agents tested in TBI models. Additionally, fentanyl may not be optimal early after TBI in humans.

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Section: Discussionmentioning

confidence: 93%

Isoflurane Improves Long-Term Neurologic Outcome Versus Fentanyl After Traumatic Brain Injury in Rats

Statler¹,

Kochanek²,

Dixon³

et al. 2000

Journal of Neurotrauma

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“…Generalized linear regression was used to look at associations between non-neurophysiological factors including initial lesion size, interval between the initial and repeat scan, the presence of a documented coagulopathy during this interval (defined as a PT > 13.5 s, aPTT > 35 s or platelets < 100/nL), and traumatic lesion growth. We also included mean CPP as another potential confounding factor, based on the concern that a relatively higher CPP target in patients with more severe intracranial injuries could contribute to hemorrhage or edema expansion [21,22]. Scatter plot matrices, Pearson correlation analyses, and linear mixed-model regression were then used to look for linear relationships between cerebrovascular reactivity metrics and lesion change in the subset of patients with intracranial recordings covering the between-scan interval.…”

Section: Discussionmentioning

confidence: 99%

Relationship Between Measures of Cerebrovascular Reactivity and Intracranial Lesion Progression in Acute TBI Patients: an Exploratory Analysis

et al. 2019

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Background: Failure of cerebral autoregulation and progression of intracranial lesion have both been shown to contribute to poor outcome in patients with acute traumatic brain injury (TBI), but the interplay between the two phenomena has not been investigated. Preliminary evidence leads us to hypothesize that brain tissue adjacent to primary injury foci may be more vulnerable to large fluctuations in blood flow in the absence of intact autoregulatory mechanisms. The goal of this study was therefore to assess the influence of cerebrovascular reactivity measures on radiological lesion expansion in a cohort of patients with acute TBI. Methods: We conducted a retrospective cohort analysis on 50 TBI patients who had undergone high-frequency multimodal intracranial monitoring and for which at least two brain computed tomography (CT) scans had been performed in the acute phase of injury. We first performed univariate analyses on the full cohort to identify nonneurophysiological factors (i.e., initial lesion volume, timing of scan, coagulopathy) associated with traumatic lesion growth in this population. In a subset analysis of 23 patients who had intracranial recording data covering the period between the initial and repeat CT scan, we then correlated changes in serial volumetric lesion measurements with cerebrovascular reactivity metrics derived from the pressure reactivity index (PRx), pulse amplitude index (PAx), and RAC (correlation coefficient between the pulse amplitude of intracranial pressure and cerebral perfusion pressure). Using multivariate methods, these results were subsequently adjusted for the non-neurophysiological confounders identified in the univariate analyses. Results: We observed significant positive linear associations between the degree of cerebrovascular reactivity impairment and progression of pericontusional edema. The strongest correlations were observed between edema progression and the following indices of cerebrovascular reactivity between sequential scans: % time PRx > 0.25 (r = 0.69, p = 0.002) and % time PAx > 0.25 (r = 0.64, p = 0.006). These associations remained significant after adjusting for initial lesion volume and mean cerebral perfusion pressure. In contrast, progression of the hemorrhagic core and extra-axial hemorrhage volume did not appear to be strongly influenced by autoregulatory status. Conclusions: Our preliminary findings suggest a possible link between autoregulatory failure and traumatic edema progression, which warrants re-evaluation in larger-scale prospective studies.

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“…However, the methodological difficulties in performing MRI in the acute phase of severe human brain trauma explain the paucity of studies particularly within the first days post-trauma and the absence of kinetics studies of edema. Contrarily, animal studies of the evolution of posttraumatic brain edema are numerous and give kinetics data [7-11], but the uses of different traumatic models, associated to secondary insults or not (i.e., hypoxia and hypotension) [7, 23,24], give rise to heterogeneous and sometimes conflicting results [7-11].…”

Section: Discussionmentioning

confidence: 99%

Dynamics of cerebral edema and the apparent diffusion coefficient of water changes in patients with severe traumatic brain injury. A prospective MRI study

et al. 2006

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The distinction between intracellular (ICE) and extracellular edema (ECE) has a crucial prognostic and therapeutic importance in patients with severe traumatic brain injury (STBI). Indeed, ICE usually leads to cellular death, and maintenance of a cerebral perfusion pressure (CPP) above 70 mmHg is still under debate since this practice may increase ECE. The purpose of this study was to describe the ECE and ICE kinetics associated with STBI using quantitative diffusion MRI. Twelve patients were prospectively studied. The initial ADC in ICE measured on day 1.3+/-0.7 is significantly reduced compared to normal-appearing parenchyma (0.51+/-0.12 * 10(-3) mm2/s vs. 0.76+/-0.03 * 10(-3) mm2/s, n=12, P<0.0001) and reaches normality on MRI 3 performed on day 14.2+/-3.3. In patients presenting an extension of ICE on MRI 2 performed on day 6.7+/-1.4 (ADC(MRI2)=0.40+/-0.11 * 10(-3) mm2/s), ADC values in the extension area at the first MRI were slightly, but not significantly reduced compared to normal parenchyma (0.69+/-0.05 * 10(-3) mm2/s, P=0.29). Normalization occurred equally by day 14. ADC in ECE (1.34+/-0.22 * 10(-3) mm2/s) was elevated and stable with time under CPP therapy. Therefore, ECE is not worsened by CCP therapy, and ICE appears more relevant than ECE in STBI.

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The Effects of Dopamine on Edema Formation in two Models of Traumatic Brain Injury

Cited by 9 publications

References 11 publications

Isoflurane Improves Long-Term Neurologic Outcome Versus Fentanyl After Traumatic Brain Injury in Rats

Isoflurane Improves Long-Term Neurologic Outcome Versus Fentanyl After Traumatic Brain Injury in Rats

Relationship Between Measures of Cerebrovascular Reactivity and Intracranial Lesion Progression in Acute TBI Patients: an Exploratory Analysis

Dynamics of cerebral edema and the apparent diffusion coefficient of water changes in patients with severe traumatic brain injury. A prospective MRI study

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