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作 者:谭延国[1] 陈瑞[2] 侯燕芝[2] 孙林[2] 于培兰[2] 刘华[2]
机构地区:[1]首都医科大学附属复兴医院检验科北京100038 [2]首都医科大学生物化学与分子生物学教研室北京100054
出 处:《中国医学物理学杂志》2004年第2期97-99,101,共4页Chinese Journal of Medical Physics
基 金:北京市教委科技发展计划基金资助项目(00KJ108)
摘 要:目的:探讨高压氧(HBO)对全脑缺血再灌注神经节苷脂(Gls)的影响。方法:实验大鼠分为缺血再灌注组(I/R组)、高压氧处理组(HBO组)及假手术组穴Sham-O组雪,以四动脉阻断法建立脑缺血再灌注模型,缺血20min,分别再灌注6h、24h、48h及96h,取全脑测定总Gls及各组份百分含量。结果:24h及48h时间点HBO组总Gls分别高于Sham-O组及对应时间点I/R组(均为p≤0.001)熏但各时间点I/R组总Gls分别同Sham-O组比无统计学变化;对I/R组而言熏GT1b百分比于再灌注24h同Sham-O组相比下降(p≤0.001),48hGD1b及GM1分别低于Sham-O组(均为p<0.05),GM3于24h高于Sham-O组及其它时间点(p≤0.001),并于96h反弹;24hHBO组GM1及GM3分别高于Sham-O组(p<0.05和p<0.01),且GD1a、GD1b和GT1b均低于Sham-O组穴p<0.01熏p<0.05和p<0.05雪,但GT1b明显高于同时相点I/R组(p<0.05)。结论:短暂全脑缺血再灌注后Gls各组份发生了改变熏提示缺血再灌注损伤机理之一为GT1b、GD1b和GM1的降低及GM3升高;HBO治疗和改善脑损伤新机理为提高脑组织Gls总量、GM1含量和加速GT1b的恢复。Purpose: To investigate effect of hyperbaric oxygen(HBO)on brain gangliosides(Gls). Method: S.D rats were devided into three groups:ischemia/reperfusion(I/R)group, group treated by HBO(HBO group) and sham-operated (Sham-O)group. Global brain ischemia was induced by a four-vessel occlusion model. Whole brain specimens were obtained and Gls and its pattern was determined at reperfusion time points of 6 h, 24 h, 48 h and 96 h after 20 minutes of ischemia. Result: Gls of HBO groups at 24 h and 48 h was higher than that of Sham-O and I/R groups of corresponding time(p≤0.001), but there was no statistical difference between Gls content of I/R groups at different time pionts and that of sham-O group. For I/R groups, GT1b proportion statistically decreased below Sham-O group at 24 h of reperfusion(p≤0.001). Both GD1b and GM1 decreased below Sham-O group at 48 h(p<0.05). GM3 of I/R group at 24 h was much higher than that of Sham-O and any other I/R groups(p≤0.001). An unknown increase of GM3 was found again at 96 h; GM1 and GM3 proportion of HBO group were higher than that of Sham-O group at 24 h (p<0.05, p<0.01), and all of GD1a? GD1b and GT1b were below Sham-O group at the same time (p<0.01, p<0.05 and p<0.05), but GT1b was statistically higher than that of I/R group at 24 h(p<0.05). Concluson: After transient whole brain I/R, the pattern of brain Gls changed. The new mechanism of neuron damage after transient whole brain I/R was the decrease of GT1b? GD1b and GM1 and increase of GM3 proportion. The new mechanism of HBO treatment to ameliorate brain I/R damage was that HBO can increase total Gls content and GM1 proportion, and accelerate GT1b restoration to normal level.
分 类 号:R743.31[医药卫生—神经病学与精神病学] O629.8[医药卫生—临床医学]
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