摘要
对１７例人脑挫裂伤的神经组织进行了超微病理及钙细胞化学的形态学观察，研究结果显示星形细胞高度肿胀、细胞器崩解，神经细胞内脂褐素增多，血脑屏障破坏，微循环障碍，兴奋性神经递质明显增多，小胶质细胞增生并迁移至神经元周围；损伤的神经组织内有多量钙离子沉积。文中结合外伤脑组织的超微形态学变化，讨论了脑损伤机制并提出了药物治疗的可能途径。
We reported the ultrastructural pathology and changes of calcium cytochemistary in neurotrauma.Brain tissue injury following CNS primary trauma results in cerebral delayed or secondary damage or slow cell death by endogenous factors.These factors include products of phospholipid hydrolysis such as free fatty acids,free radicals and excitatory amino acids as well as calcium influx. Ultrastructural demonstred cell edema and organals degeneration such as mitochondria swollen,microfilament dissolve.Microcirculate and brain blood barrier are disordes.We have found calcium deposit in cytoplasm and synaptic vesicles.A hypothesis has been proposed that,in response to primary injury,cells can produce so called “killer proteins”,which cause delayed cell death.Identification of these endogenous factors and their regulation will help to clarify mechanisms of secondary tissue damage and may lead to novel therapies.We suggested that the traumatic injury results in vasospasm and brain ischemic,alterations in mitochondrial function and reduce ATP synthesis,leading to gate openning of calcium channels,Ca influx accumulate as well as excitatory neurotransmitter release. These biocative metabolites overstimulate the phospholipase A2 and proteinase results in cytoskeleton broken,cytotoxin edema and cell membrane destory.Therefore the traumatic theaputic should be include reduce calcium ion influx and inhibited bioactive metabolites producting decreased glutamate release and block NMDA receptor as well.
出处
《电子显微学报》
CAS
CSCD
1998年第1期24-29,共6页
Journal of Chinese Electron Microscopy Society
关键词
人脑挫裂伤
超微病理
钙细胞化学
human neurotrauma\ \ ultrapathology\ \ calcium cytochemistary
