The effect of oxygen therapy on brain damage and cerebral pO2 in transient focal cerebral ischemia in the rat
The effect of oxygen therapy on brain damage and cerebral pO2 in transient focal cerebral ischemia in the rat
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DOI：
10.1088/0967-3334/28/8/017
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发表时间：
2007-08-01
影响因子：
3.2
通讯作者：
Swartz, Harold M.
中科院分区：
文献类型：
--
作者：
Hou, Huagang;Grinberg, Oleg;Swartz, Harold M.
本实验观察了高压氧（HBO）和常压氧（NBO）对局灶性脑缺血大鼠神经功能损害和脑氧合的影响。采用大鼠大脑中动脉闭塞（MCAO）再灌注模型。再灌注22 h后处死大鼠，计算梗死体积。在研究A中，HBO（2.0 ATA），NBO（100%氧气）和常压空气（NBA）在五个不同的大鼠组中各给药60分钟。在缺血期间应用HBO和NBO后的梗死面积分别为同侧非闭塞半球的8.8 ± 2.8%和22.8 ± 3.7%。缺血时应用HBO后的梗死面积明显小于NBO和NBA暴露组（p < 0.01）。在研究B中，使用电子顺磁共振（EPR）血氧仪测量了6只大鼠暴露于MCAO和HBO（2.0 ATA，60分钟）前后的脑pO（2）。缺血侧pO（2）明显下降，而对侧pO（2）保持在正常范围内。HBO暴露后几分钟进行的pO（2）测量没有显示缺血或正常半球的增加。平均相对梗死面积与研究A中观察到的变化一致。这些数据证实了HBO对脑缺血的神经保护作用，并表明在体EPR血氧测定可以作为监测缺血性脑卒中氧疗后脑氧合的有效方法。在几个部位测量pO（2）的能力提供了重要的信息，有助于优化中风高氧治疗的设计。
We examined the effect of hyperbaric oxygen ( HBO) and normobaric oxygen ( NBO) on neurologic damage and brain oxygenation before and after focal cerebral ischemia in rats. A middle cerebral artery occlusion ( MCAO)/reperfusion rat model was used. The rats were sacrificed 22 h after reperfusion, and the infarct volume was evaluated. In study A, HBO ( 2.0 ATA), NBO ( 100% oxygen) and normobaric air ( NBA) were each administered for 60 min in five different rat groups. The sizes of the infarcts after HBO and NBO applied during ischemia were 8.8 +/- 2.8% and 22.8 +/- 3.7% respectively of the ipsilateral non-occluded hemisphere. The infarct size after HBO applied during ischemia was statistically smaller than for NBO and NBA exposure ( p < 0.01). In study B, cerebral pO(2) was measured before and after MCAO and HBO exposure ( 2.0 ATA for 60 min) in six rats using electron paramagnetic resonance ( EPR) oximetry. The pO(2) in the ischemic hemisphere fell markedly following ischemia, while the pO(2) in the contralateral hemisphere remained within the normal range. Measurements of the pO(2) performed minutes after HBO exposure did not show an increase in the ischemic or normal hemispheres. The mean relative infarct size was consistent with the changes observed in study A. These data confirm the neuroprotective effects of HBO in cerebral ischemia and indicate that in vivo EPR oximetry can be an effective method to monitor the cerebral oxygenation after oxygen therapy for ischemic stroke. The ability to measure the pO(2) in several sites provides important information that should help to optimize the design of hyperoxic therapies for stroke.