摘要
本实验通过大鼠的脑损伤模型,检测了脑皮质神经元突触体胞浆中游离Ca^(2+)浓度([Ca^(2+)]i),研究神经细胞 Ca^(2+)通道变化对血脑屏障(BBB)通透性和外伤性脑水肿的影响。结果表明,脑损伤后脑突触体胞浆中游离[Ca^(2+)]i显著升高,为对照值的10～16倍。Ca^(2+)超载使BBB通透性增高,加剧脑水肿。采用Ca^(2+)拮抗剂Nimodiipine 能阻断Ca^(2+)通道开放,降低BBB通透性,对脑水肿有显著治疗效果。氢溴酸山莨菪碱的治疗作用与Nimodipine基本相同。
Experimental study of Ca^(2+) channel and itseffect on blood-brain barrier(BBB) permeabilityand brain edema following brain injury wereperformed in Wistar rats. The concentration of freeCa^(2+) ([Ca^(2+)]_i) within synaptosome of corticalneurons were detected in those animals The resultsshowed that increment of [Ca^(2+)]_i within thesynaptosomes was much more remarkable. whichwas ten to sixteen times that of control group atdifferent intervals after brain injury. Thesefindings suggested that Ca^(2+)-overload might playan important role in augmenting the BBBpermeability and aggravating brain edema. Nimodi-pine was an antagonist to Ca^(2+). Which blockedCa^(2+) channel and in turn reduced the BBB permeabi-lity and gave advantageous in treatment oftraumatic brain edema. The effect of anisodaminewas similar to that of nimodpine.
出处
《中华神经外科杂志》
CSCD
北大核心
1992年第1期41-44,T001,共5页
Chinese Journal of Neurosurgery
