Histopathological and Behavioral Effects of Immediate and Delayed Hemorrhagic Shock after Mild Traumatic Brain Injury in Rats

Histopathological and Behavioral Effects of Immediate and Delayed Hemorrhagic Shock after Mild Traumatic Brain Injury in Rats
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DOI:
10.1089/neu.2011.1979
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发表时间:
2012-01-20
影响因子:
4.2
通讯作者:
Robertson, Claudia S.
Robertson, Claudia S.
中科院分区:
医学2区
文献类型:
--
作者:
Navarro, Jovany Cruz;Pillai, Shibu;Robertson, Claudia S.

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本研究的目的是调查大脑的易感性增加,在控制轻度皮质撞击损伤后,继发性缺血性损伤。研究了初始皮质损伤后二次损伤的持续时间和时间的影响。用异氟烷麻醉的大鼠经历了3 m/s,2.5 mm变形皮质撞击损伤,然后通过从股静脉抽血诱导低血压至40 mm Hg。低血压的持续时间从40到60 mm不等。60 min低血压的时间从损伤后立即到损伤后7天不等。在损伤后2周通过行为任务和组织学检查评估结果。使用激光多普勒技术对另一组动物进行急性生理学测量,包括平均血压(MAP)、颅内压(ICP)和脑血流量(CBF)。低血压持续时间的增加导致挫伤明显扩大,从假低血压的6.5 ± 1.8 mm(3)增加到低血压60分钟的27.1 ± 3.9 mm(3)。这种恶化的挫伤,发现只有当低血压发生后立即受伤或在1小时后受伤。CA 3区神经元丢失模式相似,但损伤组间差异无统计学意义。低血压50和60分钟后,运动任务(包括平衡木平衡和平衡木行走)明显恶化。Morris水迷宫测试成绩与损伤组也有显著相关性。对急性脑血流动力学的研究表明,与接受假TBI的动物相比,接受轻度TBI的动物在低血压期间CBF的受损明显更严重。灌注不足是最严重的影响网站,但也显着在pericontusional脑。低血压50和60分钟,脑血流量没有恢复复苏后的影响网站,并恢复只是短暂的在pericontusional脑。这些结果表明,轻度TBI,如更严重的TBI水平,可以损害大脑的能力,以维持CBF在一段时间的低血压,并导致更糟糕的结果。
The purpose of this study was to investigate the increased susceptibility of the brain, after a controlled mild cortical impact injury, to a secondary ischemic insult. The effects of the duration and the timing of the secondary insult after the initial cortical injury were studied. Rats anesthetized with isoflurane underwent a 3 m/sec, 2.5-mm deformation cortical impact injury followed by hypotension to 40 mm Hg induced by withdrawing blood from a femoral vein. The duration of hypotension was varied from 40 to 60 mm. The timing of 60 min of hypotension was varied from immediately post-injury to 7 days after the injury. Outcome was assessed by behavioral tasks and histological examination at 2 weeks post-injury. A separate group of animals underwent measurement of the acute physiology including mean blood pressure (MAP), intracranial pressure (ICP), and cerebral blood flow (CBF) using a laser Doppler technique. Increasing durations of hypotension resulted in marked expansion of the contusion, from 6.5 +/- 1.8 mm(3) with sham hypotension to 27.1 +/- 3.9 mm(3) with 60 min of hypotension. This worsening of the contusion was found only when then hypotension occurred immediately after injury or at 1 h after injury. CA3 neuron loss followed a similar pattern, but the injury group differences were not significant. Motor tasks, including beam balance and beam walking, were significantly worse following 50 and 60 min of hypotension. Performance on the Morris water maze task was also significantly related to the injury group. Studies of the acute cerebral hemodynamics demonstrated that CBF was significantly more impaired during hypotension in the animals that underwent the mild TBI compared to those that underwent sham TBI. The perfusion deficit was worst at the impact site, but also significant in the pericontusional brain. With 50 and 60 min of hypotension, CBF did not recover following resuscitation at the impact site, and recovered only transiently in the pericontusional brain. These results demonstrate that mild TBI, like more severe levels of TBI, can impair the brain's ability to maintain CBF during a period of hypotension, and result in a worse outcome.