阿托伐他汀对兔动脉粥样硬化血管内皮功能的调节

The adjustment of the Atorvastatin to the endothelial function of the rabbit atherosclerotic vascular

目的探讨阿托伐他汀在兔动脉粥样硬化(Atherosclerosis,AS)一级预防中对血管内皮功能的调节。方法雄性新西兰大白兔只被随机分为动脉粥样硬化模型组(AS组)、阿托伐他汀低剂量组(LS组)和阿托伐他汀高剂量组(HS组),每组11只。所有兔子均作主动脉球囊损伤,术后第1d即开始予以下方案喂养:AS组予以高脂饲料120g/d喂养,LS组予以高脂饲料120g/d+阿托伐他汀2.5mg/d,HS组予以高脂饲料120g/d+阿托伐他汀5.0mg/d。饲养14周后全部处死。前期(球囊损伤前1d)以及后期(处死前1d)分别采静脉血检测循环中一氧化氮(Nitric oxide,NO)和内皮素(En-dothelin,ET)浓度。结果前期各组间NO、ET浓度差异无统计学意义;与前期相比,后期AS的NO明显降低及ET升高;后期时,与AS组比较,阿托伐他汀干预能使血清ET明显降低(P<0.01),NO升高(P<0.01);与低剂量组比较,高剂量组这种趋势更加明显(P<0.05)。在"球囊损伤+高脂饮食"诱导动脉粥样硬化的三组,循环中NO与ET呈负相关(r=-0.682,P<0.01)。结论血管内皮功能损害导致动脉粥样硬化的形成,阿托伐他汀干预可抑制ET分泌及促进NO分泌,从而达到调节血管内皮功能。

Objective To explore the effects atorvastatin in the regulation of vascular endothelial function for primary prevention in atherosclerosis(AS) rabbits.Methods The male New Zealand rabbits were randomly divided into atherosclerotic model group(AS group),low-dose atorvastatin group(LS group) and high-dose atorvastatin group(HS group),and each group with 11 members.All rabbits are treated as intra-aortic balloon injury.And then they began their feeding from the first day after the operation according to the following suggestion:the AS group received high-fat fodder 120g / d feeding,LS group by high-fat fodder 120g / d and atorvastatin 2.5mg / d,the HS group by high-fat fodder 120g / d and atorvastatin 5.0mg / d.14 weeks later,all of rabbits were killed.The concentration of Nitric oxide(NO) and Endothelin(ET) collected from venous blood in prophase(one day before balloon injury) and past phase(one day before death)were detected.Results In the prophase,the level of NO and ET is difference no significantly.Prophase,among the three groups show no significant difference concentrations of NO and ET.Compared with prophase,the concentration of NO is significantly reduced and ET′s is increased.at the same time,the LS group and HS group have change less than the AS group;However,the NO′s level of the AS group,LS group and the HS group in the post phase are all gradually increased(P<0.05) while the ET′s level decreased(P<0.05).further more,NO and ET was negatively correlated(r=-0.682,P<0.01).Conclusion The damage of endothelial function causes the formation of atherosclerosis;the continuing intervention of atorvastatin can inhibit ET secretion and promote NO secretion so as to adjust endothelial function.