Cerebral Ischemic Damage and Oxygen Free Radical

1)空气栓塞致短暂性脑缺血后的组织学变化（采用压缩至6 ATA的大鼠空气栓塞模型）：6 ATA空气快速减压后，血管内形成的气泡立即扰乱血脑屏障和脑微循环。光镜检查显示脑组织水肿，血管周围空间增大，神经细胞退行性变。2)缺氧猫脑氧自由基生成的来源：采用脑微透析联合高效液相色谱法研究缺氧对猫脑ECF中单胺类神经递质及其代谢物水平的影响。缺氧引起单胺代谢物（5- HIAA和HVA）立即线性下降，单胺（5- ht、NA或DA）突然增加。这些结果，再加上HVA和5-HIAA运输到脑ECF的电偶联系统的存在，表明缺氧时单胺（尤其是NA和DA）的增加或缺血可能在再氧化或再灌注期间产生更多的氧自由基。3)缺血-再灌注对大鼠脑体内原位超氧化物生成的影响：采用荧光素类似物（CLA，MCLA）作为超氧化物敏感和特异的化学发光探针和灵敏的光子计数器，研究不完全或完全脑缺血再灌注大鼠体内原位超氧化物生成。结果，再灌注后2小时内未检测到超氧化物生成增加。4)缺血再灌注在体内原位产生氧自由基：采用脑内微透析系统，检测过氧化氢作为氧自由基的制造剂，采用HPLC/异黄酮化学发光法测定大鼠完全缺血再灌注15 min或30 min脑皮质灌注液中的过氧化氢。结果表明，缺血30 min后30-90 min，大鼠过氧化氢生成增加。少

1) Histologic changes after transient brain ischemia by air embolism (using air embolism models in rats compressed to 6 ATA): After rapid decompression from 6 ATA air, the blood-brain barrier and cerebral microcirculation are immediately derranged by intra-vasculary formed air bubbles. Light microscopic examination demonstrated the edematous brain tissue with enlarged perivascular space and degenerative nerve cells.2) Origin of oxygen free radical generation in anoxic cat brain: The effect of anoxia on the levels of monoamine neurotransmitters and their metabolites in the brain ECF was studied in cats using brain microdialysis combined with HPLC. Anoxia caused an immediate linear decrease of monoamine metabolites (5- HIAA and HVA) and an abrupt increase of monoamines (5-HT, NA or DA). These results , taken together with the existence of an electrically coupled system for the transport of HVA and 5-HIAA to brain ECF, suggest that increased monoamines (especially NA and DA) during anoxia … More or ischemia possibly generate oxygen free radicals during reoxygenation or reperfusion.3) Effect of ischemia-reperfusion on superoxide generation in rat brain in vivo, in situ: Using cypridina luciferin analogus (CLA,MCLA) as sensitive and specific chemiluminescence probes for superoxide and a sensitive phooton counter, superoxide generation in vivo, in situ was investigated in rats subjected to incomplete or complete brain ischemia followed by reperfusion. As a result, increased superoxide generation was not detected within 2 hours after reperfusion.4) Oxygen free radical generation in vivo, in situ by ischemia-reperfusion: Using brain in vivo microdialysis system and detecting hydrogen peroxide as a maker of oxygen free radical, hydrogen peroxide in perfusate from the brain cortex was measured by a HPLC/isoluminol chemiluminescence assay in rats subjected to 15 or 30 min complete ischemia followed by reperfusion. As results, 30-90 min after reperfusion, increased hydrogen peroxide generation was detected in rats subjected to 30 min ischemia. Less