Dietrich W D, Alonso O, Busto R, Prado R, Zhao W, Dewanjee M K, Ginsberg M D
Department of Neurology, Neurotrauma Disease Research Center, University of Miami School of Medicine, Florida 33101, USA.
Neurosurgery. 1998 Sep;43(3):585-93; discussion 593-4. doi: 10.1097/00006123-199809000-00105.
Mild-to-moderate reductions in local cerebral blood flow (ICBF) have been reported to occur in rats after moderate (1.7-2.2 atm) fluid percussion brain injury. The purpose of this study was to determine whether evidence for severe ischemia (i.e., mean ICBF < 0.25 ml/g/min) could be demonstrated after severe brain injury. In addition, patterns of indium-labeled platelet accumulation and histopathological outcome were correlated with the hemodynamic alterations.
Sprague-Dawley rats (n = 23), anesthetized with halothane and maintained on a 70:30 mixture of nitrous oxide:oxygen and 0.5% halothane, underwent normothermic (37 degrees C) parasagittal fluid percussion brain injury (2.4-2.6 atm). Indium-111-tropolone-labeled platelets were injected 30 minutes before traumatic brain injury (TBI), while 14C-iodoantipyrine was infused 30 minutes after trauma for ICBF determination. Sham-operated animals (n = 8) underwent similar surgical procedures but were not injured. For histopathological analysis, traumatized rats (n = 5) were perfusion-fixed 3 days after TBI.
In autoradiographic images of indium-labeled platelets, abnormal platelet accumulation that was most pronounced overlying the pial surface was commonly associated with severe reductions in ICBF within underlying cortical regions 30 minutes after TBI. For example, within the lateral parietal cortex, ICBF was significantly reduced from 1.67 +/- 0.11 ml/g per minute (mean +/- standard error of the mean) in sham-operated animals to 0.23 +/- 0.03 ml/g per minute within the traumatized group. In addition to focal severe ischemia, moderate reductions in ICBF were detected throughout the traumatized hemisphere, including the frontal and occipital cortices, hippocampus, thalamus, and striatum. Mild decreases in ICBF were also observed throughout the contralateral cerebral cortex. At 3 days after severe TBI, histopathology demonstrated intracerebral and subarachnoid hemorrhage associated with cerebral contusion and selective neuronal necrosis.
These data indicate that multiple cerebrovascular abnormalities, including subarachnoid hemorrhage, focal platelet accumulation, and severe ischemia, are important early events in the pathogenesis of cortical contusion formation after TBI. Injury severity is expected to be a critical factor in determining what therapeutic strategies are attempted in the clinical setting.
据报道，在大鼠遭受中度（1.7 - 2.2个大气压）液体冲击性脑损伤后，局部脑血流量（ICBF）会出现轻度至中度降低。本研究的目的是确定在重度脑损伤后是否能证实存在严重缺血的证据（即平均ICBF < 0.25 ml/g/min）。此外，将铟标记血小板的聚集模式和组织病理学结果与血流动力学改变相关联。
23只Sprague-Dawley大鼠，用氟烷麻醉，维持在氧化亚氮：氧气70:30的混合气体和0.5%氟烷条件下，接受常温（37℃）矢状旁液体冲击性脑损伤（2.4 - 2.6个大气压）。在创伤性脑损伤（TBI）前30分钟注射铟 - 111 - 托酚酮标记的血小板，而在创伤后30分钟输注14C - 碘安替比林用于测定ICBF。假手术动物（n = 8）接受类似的外科手术但未受伤。为进行组织病理学分析，创伤大鼠（n = 5）在TBI后3天进行灌注固定。
在铟标记血小板的放射自显影图像中，TBI后30分钟，最明显覆盖在软脑膜表面的异常血小板聚集通常与下方皮质区域ICBF的严重降低相关。例如，在外侧顶叶皮质，ICBF在假手术动物中从每分钟1.67±0.11 ml/g（平均值±平均标准误差）显著降低至创伤组中的每分钟0.23±0.03 ml/g。除了局灶性严重缺血外，在整个创伤半球，包括额叶和枕叶皮质、海马、丘脑和纹状体，均检测到ICBF中度降低。在对侧大脑皮质也观察到ICBF轻度降低。在重度TBI后3天，组织病理学显示脑内和蛛网膜下腔出血，伴有脑挫伤和选择性神经元坏死。
这些数据表明，多种脑血管异常，包括蛛网膜下腔出血、局灶性血小板聚集和严重缺血，是TBI后皮质挫伤形成发病机制中的重要早期事件。损伤严重程度预计是决定在临床环境中尝试何种治疗策略的关键因素。
