摘要
本文应用针形微型氧电极动态观察了猫局部脑缺血状态下大脑组织缺血区组织氧分压(PtO_2)改变,并分析PtO_2与相应部位体感诱发电位(SEP)的关系.实验中观察到,结扎一侧MCA后缺血区大脑组织不同深度的缺氧程度不同,表现为浅层皮质(0～1000μm)PtO_2下降较明显(缺血前平均5.1kPa,缺血后0.5h下降到2.9kPa,n=6,P<0.05),而深层大脑组织(1001～5000μm)PtO_2改变不明显.SEP在缺血后其振幅明显下降(P<0.05),但中枢传导时间改变不明显.在动态观察中,缺血后期(1.5,3.0h)PtO_2平均值有所回升,而SEP没有得到改善,可能因缺血后缺氧所致的细胞损伤,虽然在后期因侧枝循环等因素使氧得到重新分布,但不足以使神经元电活动得到改善.
Tissue oxygen pressure (PtO_2) and somatosensory-evoked potentials (SEP) in the cat brain and their relationship were analysed during experimental focal cerebral ischemia. PtO_2 was determined by an oxygen micro electrode in the parietal brain of cats. Ischemia was induced in 6 cats for 3.0h, by clamping the right middle cerebral artery (MCA) . The results showed marked decrease of PtO_2 in the superficial layer of cortex (depth of 0 to 1000μm, from average 5.1 to 2.9 kPa, n=6, P<0.05) 0.5h after MCA clamped but no significant lowering of mean PtO_2 values in the deeper brain (1001 to 5000μm) was observed. At the same time, the amplitudes of SEP also decreased significantly after MCA clamped, while the conduction time of SEP showed no obvious change. Results also showed slight elevation in the mean PtO_2 values in the ischemic area in the later periods of ischemia, without improvement in the amplitudes of SEP, suggesting that the ischemia induced cell damage, regardless of oxygen supply redistribution prohibited the improvement of the electric activity of neurons in the ischemic area.
关键词
脑缺血
氧分压
诱发电位
Evoked potentials
somatosensory
Oxygen partial pressure
Cat
Cerebral ischemia/physiopathol
Cerebral anoxia/physiopathol
Oxygen microeletrode
