Matsushita Y, Bramlett H M, Kuluz J W, Alonso O, Dietrich W D
The Neurotrauma Research Center, University of Miami School of Medicine, FL, USA.
J Cereb Blood Flow Metab. 2001 Jul;21(7):847-56. doi: 10.1097/00004647-200107000-00010.
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 mm(3) vs. 2.02 +/- 0.51 mm(3), mean +/- SD, P < 0.05). These findings demonstrate that mild hemorrhagic hypotension after FP injury worsens local histopathologic outcome, possibly through vascular mechanisms.
创伤性脑损伤（TBI）后大脑自动调节和脑血管反应性的改变可能会增加大脑对包括动脉低血压在内的继发性损伤的易感性。本研究的目的是评估轻度出血性低血压对TBI后血流动力学和组织病理学结果的影响。将插管麻醉的雄性大鼠进行中度（1.94至2.18大气压）矢状旁流体冲击（FP）脑损伤。TBI后，动物被分为正常血压组（第1组：仅TBI，n = 6）或低血压组（第2组：TBI +低血压，n = 6）。在TBI或假手术操作5分钟后，通过出血诱导中度低血压（60 mmHg/30分钟）。假手术对照组（第3组，n = 7）经历诱导性低血压期，而正常血压对照组（第4组，n = 4）则不经历。为了测量局部脑血流量（rCBF），在TBI前、TBI后20分钟和60分钟注射放射性微球（n = 23）。为了进行定量组织病理学评估，在TBI后3天对单独的动物组进行灌注固定（n = 22）。在TBI后20分钟，在正常血压条件下，皮质和皮质下脑区的rCBF分别双侧降低了57%±6%和48%±11%。与正常血压的TBI大鼠相比，在组织病理学易损的（P1）顶叶后皮质中，诱导性低血压导致的血流动力学抑制明显更大（P < 0.01）。与正常血压的TBI大鼠相比，继发性低血压还增加了特定前囟水平的挫伤面积（P < 0.05），以及总体挫伤体积（0.96±0.46 mm³对2.02±0.51 mm³，平均值±标准差，P < 0.05）。这些发现表明，FP损伤后轻度出血性低血压可能通过血管机制恶化局部组织病理学结果。
