摘要
通过检测脑皮质神经元突触体胞浆游离Ca2+浓度([Ca2+]i),研究大鼠脑损伤后神经细胞Ca2+通道变化,及其对血脑屏障(BBB)和脑水肿的影响。结果表明,脑损伤后突触体[Ca2+]i显著升高,分别为对照值的10~17倍,证实了神经细胞ca2+超载可能是引起BBB通透增加,加剧脑水肿的重要因素。钙通过阻断剂尼莫地平可阻止Ca2+通道开放,有利于脑水肿防治。
The
authors investigated the changes of ca2+ channel in the cortical neurons and the effect on
blood-brain barrier(BBB) perme- ability and cerebral edema by detecting the concentration of
the cytosolic free Ca2+([Ca2+]i) within synaptosome of the neurons fol-lowing brain injury in 224
Wistar rats. The results showed that the increase of[Ca2+]i within synaptosomes was
remarkable. It was10-16 times of the control values at different intervals after brain injury.These
findings indicate that the Ca2+-overload might play animportant role in the increase of BBB
permeability and aggravate the cerebral edema and nimodipine could block the neuronal
Ca2+channel hence was favovable to the treatment of traumatic cerebral edema.
出处
《第一军医大学学报》
CSCD
1994年第1期6-8,共3页
Journal of First Military Medical University
关键词
颅脑损伤
脑水肿
钙通道
血脑屏障
brain
injury
cerebral edema
Ca2+channel
blood-brain barrier
nimodipine