TY - JOUR
T1 - Widespread hemodynamic depression and focal platelet accumulation after fluid percussion brain injury
T2 - A double-label autoradiographic study in rats
AU - Dalton Dietrich, W.
AU - Alonso, Ofelia
AU - Busto, Raul
AU - Prado, Ricardo
AU - Dewanjee, Sumit
AU - Dewanjee, Mrinal K.
AU - Ginsberg, Myron D.
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 1996
Y1 - 1996
N2 - Cerebrovascular damage leading to subsequent reductions in local cerebral blood flow (ICBF) may represent an important secondary injury mechanism following traumatic brain injury (TBI). We determined whether patterns of 111indium-labeled platelet accumulation were spatially related to alterations in ICBF determined autoradiographically 30 min after TBI. Sprague-Dawley rats (n = 8), anesthetized with halothane and maintained on a 70:30 (vol/vol) mixture of nitrous oxide/oxygen and 0.5% halothane, underwent parasagittal fluid percussion brain injury (1.7-2.2 atm). 111Indium- tropolone-labeled platelets were injected 30 min prior to TBI while [14C]- iodoantipyrine was infused 30 min after trauma. Sham-operated animals (n = 7) underwent similar surgical procedures but were not injured. In autoradiographic images of the indium-labeled platelets, focal sites of platelet accumulation within the traumatized hemisphere were restricted to the pial surface (five of eight rats), the external capsule underlying the lateral parietal cortex (five of eight rats), and within cerebrospinal fluid (CSF) compartments (six of eight rats). In contrast, mild-to-moderate reductions in ICBF, not restricted to sites of platelet accumulation, were seen throughout the traumatized hemisphere. Flow reductions were most severe in coronal sections underlying the impact site. For example, within the lateral parietal cortex and hippocampus, ICBF was significantly reduced [p < 0.01; analysis of variance (ANOVA)] from 1.71 ± 0.34 (mean ± SD) and 0.78 ± 0.12 ml/g/min, respectively, versus 0.72 ± 0.17 and 0.41 ± 0.06 ml/g/min within the traumatized hemisphere. Significant flow reductions were also seen in remote cortical and subcortical areas, including the right frontal cortex and striatum. These results indicate that focal platelet accumulation and widespread hemodynamic depression are both early consequences of TBI. Therapeutic strategies directed at these early microvascular consequences of TBI may be neuroprotective by attenuating secondary ischemic processes.
AB - Cerebrovascular damage leading to subsequent reductions in local cerebral blood flow (ICBF) may represent an important secondary injury mechanism following traumatic brain injury (TBI). We determined whether patterns of 111indium-labeled platelet accumulation were spatially related to alterations in ICBF determined autoradiographically 30 min after TBI. Sprague-Dawley rats (n = 8), anesthetized with halothane and maintained on a 70:30 (vol/vol) mixture of nitrous oxide/oxygen and 0.5% halothane, underwent parasagittal fluid percussion brain injury (1.7-2.2 atm). 111Indium- tropolone-labeled platelets were injected 30 min prior to TBI while [14C]- iodoantipyrine was infused 30 min after trauma. Sham-operated animals (n = 7) underwent similar surgical procedures but were not injured. In autoradiographic images of the indium-labeled platelets, focal sites of platelet accumulation within the traumatized hemisphere were restricted to the pial surface (five of eight rats), the external capsule underlying the lateral parietal cortex (five of eight rats), and within cerebrospinal fluid (CSF) compartments (six of eight rats). In contrast, mild-to-moderate reductions in ICBF, not restricted to sites of platelet accumulation, were seen throughout the traumatized hemisphere. Flow reductions were most severe in coronal sections underlying the impact site. For example, within the lateral parietal cortex and hippocampus, ICBF was significantly reduced [p < 0.01; analysis of variance (ANOVA)] from 1.71 ± 0.34 (mean ± SD) and 0.78 ± 0.12 ml/g/min, respectively, versus 0.72 ± 0.17 and 0.41 ± 0.06 ml/g/min within the traumatized hemisphere. Significant flow reductions were also seen in remote cortical and subcortical areas, including the right frontal cortex and striatum. These results indicate that focal platelet accumulation and widespread hemodynamic depression are both early consequences of TBI. Therapeutic strategies directed at these early microvascular consequences of TBI may be neuroprotective by attenuating secondary ischemic processes.
KW - Brain trauma
KW - Cerebral blood flow
KW - Platelets
KW - Vasoactive substances
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U2 - 10.1097/00004647-199605000-00015
DO - 10.1097/00004647-199605000-00015
M3 - Article
C2 - 8621753
AN - SCOPUS:9244243663
VL - 16
SP - 481
EP - 489
JO - Journal of Cerebral Blood Flow and Metabolism
JF - Journal of Cerebral Blood Flow and Metabolism
SN - 0271-678X
IS - 3
ER -