目的：探讨慢性心理应激诱发动脉粥样硬化（ AS）的可能机制。方法将160只健康雄性新西兰兔随机分为对照组、高脂组应激组、应激＋高脂组各40只。对照组及应激组予普通饲料喂养，高脂组、应激＋高脂组予高脂饲料喂养；应激组及应激＋高脂组均予旋转、噪音、惊恐、断食、断水等刺激致心理应激制备AS模型；共16周。于制模前及制模第4、8、12、16周末测定各组血脂（包括TC、TG、LDL-c、HDL-c）；分离腹主动脉组织行油红O染色，观察脂质沉积情况。结果第4、8周血脂水平应激＋高脂组＞高脂组＞应激组（ P＜0．05）；第12、16周末，与对照组比较，应激组HDL-c水平明显下降（P＜0．05），其余指标明显升高（P＜0．05）；高脂组与应激组LDL-c水平无统计学差异，其余指标均明显升高（P＜0．05）；与高脂组比较，应激＋高脂组HDL-c明显降低（P＜0．05），其余指标均明显升高（P＜0．05）。脂质沉积情况：应激＋高脂组、高脂组、应激组分别于第4、8、12周开始有脂质沉积，第16周应激＋高脂组＞高脂组＞应激组（P＜0．05）。结论慢性心理应激诱导的AS脂质紊乱特征与高脂所致的AS的机制不同，其促进AS形成的机制可能为引起LDL-c水平升高、HDL-c降低。%Objective To investigate the clinical features of atherosclerosis ( AS) induced by chronic psychological stress ( CPS) and the possible mechanism .Methods Totally 160 New Zealand male rabbits were randomly divided into 4 groups, 40 cases in each group:the control group (group C), CPS group, high cholesterol feed group (HCF group) and chronic stress plus high cholesterol feed group ( CPS+HCF group ) .Rabbits in the C and CPS groups were fed with stand-ard diet;HCF and CPS+HCF groups were fed with high-fat diet.Rabbits in the CPS and CPS+HCF groups underwent ro-tation, noise, panic, fasting and water stimulation to induce the psychological stress in order to prepare the AS models .The experiment lasted for 16 weeks.The concentrations of TC , TG, LDL-c, HDL-c and abdominal aorta of the rabbits stained by oil red O were examined before modeling and after 4, 8, 12 and 16 weeks respectively .Results At week 4 and 8, the concentrations of TC, TG, LDL-c and HDL-c:CPS+HCF group >HCF group >CPS group (P<0.05).At the end of 12th and 16th weeks, the serum HDL-c level of group CPS decreased significantly as compared with that of group C (P<0.05), and the rest indexes increased significantly (P<0.05); the serum LDL-c level had no statistical difference be-tween the CPS and HCF groups (P>0.05), and the other indexes decreased significantly (P<0.05);the serum HDL-c level of group CPS+HCF significantly decreased as compared with that of group HCF (P<0.05), and the other indexes increased (P<0.05).The lipidoses in arterial wall of CPS +HCF group (after 4 weeks), HCF group (after 8 weeks) and CPS group (after 12 weeks) were observed.After 16 weeks, HCF group exhibited more lipidoses in arterial wall than CPS group and CPS+HCF group exhibited more lipidoses than HCF group ( all P<0.05) .Conclusion The features of blood lipids metabolic disorders of AS induced by CPS are different from that induced by HCF .CPS maybe contributes to AS by increasing LDL-c level and decreasing HDL-c level.
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