摘要
目的 通过应用激光共聚焦显微镜检测活体脑片Ca2 + 荧光强度来探讨停循环后脑损伤的机制。方法 将 16只小型幼猪分别经过单纯深低温停循环 (DHCA)或上腔静脉逆行灌注 (RCP)90min后复灌 12 0min。制备活体脑片 ,检测脑片Ca2 + 荧光强度 ,并进行组织病理和电子显微镜检查。结果 RCP组小脑Ca2 + 荧光强度灰度值为 9± 4 ,DHCA组为 32± 2 1,两者比较P <0 .0 0 1;视网膜Ca2 +荧光强度灰度值为 2 1± 14 ,DHCA组为 4 4± 2 1,两者比较P <0 .0 5。相关分析显示活体脑片Ca2 + 荧光强度与中重度嗜酸性变性有相关性 (r =0 .86 1,P <0 .0 5 )。结论 Ca2 + 超载参与了DHCA后神经细胞的损伤过程 ,RCP能明显减轻Ca2 + 超载 。
Objective To examine the calcium fluorescent intensity of vital brain slice and study the mechanism of brain injury after circulatory arrest. Methods Eight pigs underwent 90 minutes′ deep hypothermic circulation arrest (DHCA) and eight pigs underwent retrograde cerebral perfusion (RCP) through superior vena cava and then rewarmed for 120 minutes. Vital brain slices were obtained and the calcium fluorescent intensity was examined with laser confocal scanning microscope (LCSM). The morphological change was examined with light microscope and electron microscope. Results The calcium fluorescent intensity of vital brain slice was lower in RCP group than in DHCA group. The calcium fluorescent intensity of vital brain slice is correlated with the level of moderate and severe eosinophilic degeneration of neuron ( r =0.86, P <0.05). Conclusion Calcium overload contributes to the injury of neuron after DHCA. RCP remarkably attenuates calcium overload, thus protecting the brain tissue.
出处
《中华医学杂志》
CAS
CSCD
北大核心
2002年第1期27-30,共4页
National Medical Journal of China
基金
国家自然科学基金资助项目 (3 9770 73 3 )
