Effect of hypoxia on traumatic brain injury in rats: Part 1. Changes in neurological function, electroencephalograms, and histopathology.
Effect of hypoxia on traumatic brain injury in rats: Part 1. Changes in neurological function, electroencephalograms, and histopathology.
复制标题
缺氧对大鼠脑外伤的影响：第1部分：神经功能、脑电图和组织病理学的变化。
作者：
N. Ishige;L. Pitts;T. Hashimoto;M. Nishimura;H. Bartkowski
评估了缺氧对头部受伤大鼠的神经功能、压缩频谱阵列脑电图和组织病理学的影响。低氧损伤（PaO2，40 mm Hg，持续 30 分钟）本身并不会引起神经功能缺损。受到 5 个大气压颞部液体撞击损伤的大鼠中，20% 的大鼠在撞击侧出现偏瘫，而 80% 的大鼠在损伤 24 小时后没有出现偏瘫。然而，70%同时患有液体冲击损伤和缺氧损伤的大鼠要么出现明显的偏瘫，要么表现出无自发运动，要么死亡（P小于0.02）。单独的撞击会产生脑电图功率的最初抑制，在缺氧损伤的大鼠中这种抑制会持续较长时间。最显着的影响出现在受伤的半球，而对侧半球的影响较短且不太严重。用氯化 2,3,5-三苯基四唑对体内损伤的脑组织进行灌注染色，显示缺氧损伤大鼠的撞击部位周围存在广泛的缺血区域。在单独受到冲击损伤或缺氧的大鼠中不存在该缺血区域。我们得出的结论是，创伤后缺氧明显增加了该大鼠模型中冲击损伤的严重程度。这些发现表明，头部受伤患者中常见的缺氧很可能会恶化冲击损伤的效果，并且可能是严重颅脑外伤患者弥漫性神经功能障碍的主要原因。
The effect of hypoxia on neurological function, compressed spectral array electroencephalography, and histopathology in head-injured rats was evaluated. By itself, an hypoxic insult (PaO2, 40 mm Hg for 30 minutes) caused no neurological deficit. Twenty per cent of rats injured by a 5-atmosphere temporal fluid percussion impact were hemiparetic contralateral to the side of impact, whereas 80% had no deficit 24 hours after injury. Seventy per cent of rats with both fluid impact injury and hypoxic insult, however, either had a definite hemiparesis, showed no spontaneous movement, or died (P less than 0.02). Impact alone produced an initial depression in electroencephalogram power that was prolonged in rats with hypoxic insult; the most dramatic effect was found in the injured hemisphere, with shorter and less profound effects in the contralateral hemisphere. Perfusion staining of injured cerebral tissue in vivo with 2,3,5-triphenyltetrazolium chloride showed an area of extensive ischemia around the impact site in rats with hypoxic insult. This ischemic area was not present in rats with either impact injury or hypoxia alone. We conclude that posttraumatic hypoxia clearly increases the severity of impact injury in this rat model. These findings suggest that hypoxia, which is common in head-injured patients, very likely worsens the effect of impact injury and may account for much of the diffuse neurological dysfunction in patients with severe craniocerebral trauma.