THE EFFECT OF HYPOXIA ON TRAUMATIC HEAD-INJURY IN RATS - ALTERATIONS IN NEUROLOGIC FUNCTION, BRAIN EDEMA, AND CEREBRAL BLOOD-FLOW
THE EFFECT OF HYPOXIA ON TRAUMATIC HEAD-INJURY IN RATS - ALTERATIONS IN NEUROLOGIC FUNCTION, BRAIN EDEMA, AND CEREBRAL BLOOD-FLOW
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DOI：
10.1038/jcbfm.1987.131
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发表时间：
1987-12-01
影响因子：
6.3
通讯作者：
WEINSTEIN, PR
中科院分区：
文献类型：
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作者：
ISHIGE, N;PITTS, LH;WEINSTEIN, PR
我们评估了创伤后早期缺氧对脑损伤大鼠神经功能、磁共振成像（MRI）、脑组织比重和脑血流量（CBF）的影响。缺氧损伤（PaO2 40 mm Hg，持续30分钟）对脑功能的任何测量几乎没有影响。然而，颞部液压冲击损伤后，缺氧显著增加发病率。受撞击的大鼠（4.9 . ±. 0.3大气压）加缺氧时，71%的大鼠在伤后24小时出现撞击侧对侧运动无力，而仅29%的大鼠受到撞击后出现明显无力（P < 0.05）。损伤后24小时的MR图像上观察到的病变仅限于大鼠撞击损伤的撞击部位，但在大鼠撞击损伤和缺氧损伤的同侧皮质中观察到广泛的T1弛豫时间较长的区域。脑组织比重测定结果表明，在大鼠撞击伤和缺氧时，脑水肿更广泛和严重。损伤后24小时进行的[14C]碘安替比林放射自显影显示，在具有撞击损伤和缺氧的大鼠中，整个同侧皮质存在广泛的低灌注。这些结果表明，大面积的冲击损伤的大脑是非常容易受到二次损伤，可以不可挽回地损害神经组织，并提供实验证据，观察到的不良影响缺氧对结果后，人类头部损伤。
We evaluated the effects of early posttraumatic hypoxia on neurologic function, magnetic resonance images (MRI), brain tissue specific gravities, and cerebral blood flow (CBF) in head-injured rats. By itself, an hypoxic insult (PaO2 40 mm Hg for 30 min) had little effect on any measure of cerebral function. After temporal fluid-percussion impact injury, however, hypoxia significantly increased morbidity. Of rats subjected to impact (4.9 .+-. 0.3 atm) plus hypoxia, 71% had motor weakness contralateral to the impact side 24 h after injury, while only 29% of rats subjected to impact alone had demonstrable weakness (p < 0.05). Lesions observed on MR images 24 h after injury were restricted to the impact site in rats with impact injury alone, but extensive areas with longer T1 relaxation times were observed throughout the ipsilateral cortex in rats with impact injury and hypoxic insult. Brain tissue specific gravity measurements indicated that much more widespread and severe edema developed in rats with impact injury and hypoxia. [14C]Iodoantipyrine autoradiography performed 24 h after injury showed that there was extensive hypoperfusion of the entire ipsilateral cortex in rats with impact injury and hypoxia. These results show that large areas of impact-injured brain are extremely vulnerable to secondary insults that can irreparably damage neural tissue, and provide experimental evidence for the observed adverse effects of hypoxia on outcome after human head injury.