Dietrich W D, Alonso O, Busto R, Prado R, Dewanjee S, Dewanjee M K, Ginsberg M D
Neurotrauma Clinical Research Center, Department of Neurology, University of Miami School of Medicine, Florida, USA.
J Cereb Blood Flow Metab. 1996 May;16(3):481-9. doi: 10.1097/00004647-199605000-00015.
Cerebrovascular damage leading to subsequent reductions in local cerebral blood flow (lCBF) may represent an important secondary injury mechanism following traumatic brain injury (TBI). We determined whether patterns of 111-indium-labeled platelet accumulation were spatially related to alterations in lCBF 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). 111-Indium-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 lCBF, 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, lCBF 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.
导致局部脑血流量（lCBF）随后减少的脑血管损伤可能是创伤性脑损伤（TBI）后一种重要的继发性损伤机制。我们确定了111-铟标记血小板聚集模式是否与TBI后30分钟通过放射自显影术测定的lCBF改变在空间上相关。用氟烷麻醉的Sprague-Dawley大鼠（n = 8），维持在70:30（体积/体积）的一氧化二氮/氧气和0.5%氟烷混合气体中，接受矢状旁流体冲击性脑损伤（1.7 - 2.2大气压）。在TBI前30分钟注射111-铟-托酚酮标记的血小板，而在创伤后30分钟输注[14C]-碘安替比林。假手术动物（n = 7）接受类似的手术操作但未受伤。在铟标记血小板的放射自显影图像中，受伤半球内血小板聚集的局灶部位局限于软脑膜表面（8只大鼠中的5只）、顶叶外侧皮质下方的外囊（8只大鼠中的5只）以及脑脊液（CSF）腔室（8只大鼠中的6只）。相比之下，在整个受伤半球均可见lCBF有轻度至中度降低，且不限于血小板聚集部位。血流减少在撞击部位下方的冠状切片中最为严重。例如，在顶叶外侧皮质和海马体内，lCBF分别从1.71±0.34（平均值±标准差）和0.78±0.12毫升/克/分钟显著降低[p <0.01；方差分析（ANOVA）]，而在受伤半球内分别为0.72±0.17和0.41±0.06毫升/克/分钟。在包括右侧额叶皮质和纹状体在内的远隔皮质和皮质下区域也可见显著的血流减少。这些结果表明，局灶性血小板聚集和广泛的血流动力学抑制都是TBI的早期后果。针对TBI这些早期微血管后果的治疗策略可能通过减轻继发性缺血过程而具有神经保护作用。
