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增强型体外反搏对高胆固醇血症猪血小板膜流动性和脂质过氧化的影响
引用本文:熊艳,詹红,王伟袆,何小洪,罗景云,陈国伟,郑振声,伍贵富. 增强型体外反搏对高胆固醇血症猪血小板膜流动性和脂质过氧化的影响[J]. 中华生物医学工程杂志, 2010, 16(5). DOI: 10.3760/cma.j.issn.1674-1927.2010.05.003
作者姓名:熊艳  詹红  王伟袆  何小洪  罗景云  陈国伟  郑振声  伍贵富
作者单位:1. 中山大学附属第一医院急诊科,广州,510080
2. 广州市天河区红十字会医院
3. 中山大学卫生部辅助循环重点实验室
4. 中山大学附属第一医院心血管医学部心内科,广州,510080
基金项目:广东省教育厅产学研结合示范基地项目,广东省科技计划重点项目,中山大学青年教师科研启动基金
摘    要:目的 研究增强型体外反搏对高胆固醇血症猪血小板膜流动性和脂质过氧化的影响,并探讨增强型体外反搏抗动脉粥样硬化的机制.方法 18头雄性乳猪随机分为正常饲养组(n=6)、高脂饲养组(n=6)及高脂饲养+体外反搏组(n=6),后2组通过高脂饲养复制高胆固醇血症猪模型并对高脂饲养+体外反搏组进行每次2 h,隔日1次,共计36 h的增强型体外反搏干预.分别于分组饲养前、反搏前、反搏中期(反搏进行18 d)和反搏结束(反搏进行36d)时留取3组动物静脉血,测定总胆固醇(Chol)、低密度脂蛋白(LDL)和脂质过氧化水平,并用Caimi法检测血小板膜流动性指标荧光偏振度P'.结果 与正常饲养组比较,反搏前、反搏中期和反搏结束时高脂饲养组和高脂饲养+体外反搏组血清Chol和LDL明显升高(均P<0.05).3组P'和脂质过氧化水平在分组饲养前无显著差异(P>0.05);反搏前、反搏中期和反搏结束时,高脂饲养组与高脂饲养+体外反搏组P'和脂质过氧化水平较正常饲养组同时期均有显著增高(均P<0.05);反搏中期和反搏结束时高脂饲养+体外反搏组P'和脂质过氧化水平较高脂饲养组显著降低[P':(0.451±0.047)比(0.655±0.034),(0.561±0.043)比(0.723±0.050);脂质过氧化水平:(0.56±0.06)mmol/L比(0.88±0.07)mmol/L,(0.72±0.13)mmol/L比(1.23±0.11)mmol/L,均P<0.05].结论 增强型体外反搏可能通过减少脂质过氧化,改善血小板膜流动性阻遏高胆固醇血症的病理生理进程,这可能是其发挥抗动脉粥样硬化的机制之一.

关 键 词:反搏动术,体外  高胆固醇血症  血小板膜流动性  脂质过氧化作用  动脉粥样硬化

Effects of enhanced external counterpulsation on platelet membrane fluidity and lipid peroxidation in hypercholesterolemic pigs
XIONG Yan,ZHAN Hong,WANG Wei-yi,HE Xiao-hong,LUO Jing-yun,CHEN Guo-wei,ZHENG Zhen-sheng,WU Gui-fu. Effects of enhanced external counterpulsation on platelet membrane fluidity and lipid peroxidation in hypercholesterolemic pigs[J]. Chinese Journal of Biomedical Engineering, 2010, 16(5). DOI: 10.3760/cma.j.issn.1674-1927.2010.05.003
Authors:XIONG Yan  ZHAN Hong  WANG Wei-yi  HE Xiao-hong  LUO Jing-yun  CHEN Guo-wei  ZHENG Zhen-sheng  WU Gui-fu
Abstract:Objective To explore the effect of enhanced external counterpulsation (EECP) on platelet membrane fluidity and lipid peroxidation in hypercholesterolemic pigs, and to investigate the mechanisms by which EECP acts against artherosclerosis. Methods Eighteen male infant pigs were randomly divided into 3 groups according to their diet: the normal diet control group (n=6) , the hypercholesterolemia control group (n=6) and the hypercholesterolemia + EECP group (n=6). After porcine hypercholesterolemia model was established in the latter two groups, EECP was given to the hypercholesterolemia+EECP group by 2 h per session, once every two days, for up to 36 h. Blood samples were collected from all the animals to measure the levels of total cholesterol (Chol), low density lipoprotein (LDL) and lipid peroxidation before hypercholesterolemia modeling, prior to EECP treatment, during the EECP treatment (on day 18) and after completion of EECP treatment (on day 36). In addition, platelet membrane fluidity as reflected by fluorescence polarizability (P') was measured according to Caimi's methods. Results The levels of Chol and LDL were significantly higher in hypercholesterolemic pigs with or without EECP treatment compared with normal diet control group before, during and after EECP (all P<0.05), whereas there were no significant differences in P' and lipid peroxidation among 3 groups before allocation to different diets (P>0.05). The fluorescence polarizability P' and level of lipid peroxidation were remarkably elevated in both hypercholesterolemia control group and the hypercholesterolemia+EECP group before, during and after EECP compared with the normal diet control group at the same time points (all P<0.05) , and were remarkably lowered in the hypercholesterolemia + EECP group compared with hypercholesterolemia control group during and after EECP[P':(0.451 ±0.047)vs(0.655±0.034), (0.561±0.043) vs (0.723±0.050) ;lipid peroxidation: (0.56±0.06)mmol/L vs (0.88±0.07)mmol/L, (0.72±0.13)mmol/L vs( 1.23±0.11 )mmol/L, all P<0.05]. Conclusion EECP may lead to reduced lipid peroxidation and improve platelet membrane fluidity, and thereby delay the pathophysiological progression of hypercholesterolemia, which might be one of mechanisms of its anti-atherosclerotic effect.
Keywords:External counterpulsation  Hypercholesterolemia  Platelet membrane fluidity  Lipid peroxidation  Atherosclerosis
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