脑损伤后神经细胞Ca^（2＋）通道变化及其对BBB和脑水肿的影响

The changes of neuronal Ca2+channel and effect on BBB permeability and cerebral edema associated with brain injury

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.