CAJ | 학술논문

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.
목적 연구증강형체외반박대고담고순혈증저혈소판막류동성화지질과양화적영향,병탐토증강형체외반박항동맥죽양경화적궤제.방법 18두웅성유저수궤분위정상사양조(n=6)、고지사양조(n=6)급고지사양+체외반박조(n=6),후2조통과고지사양복제고담고순혈증저모형병대고지사양+체외반박조진행매차2 h,격일1차,공계36 h적증강형체외반박간예.분별우분조사양전、반박전、반박중기(반박진행18 d)화반박결속(반박진행36d)시류취3조동물정맥혈,측정총담고순(Chol)、저밀도지단백(LDL)화지질과양화수평,병용Caimi법검측혈소판막류동성지표형광편진도P'.결과 여정상사양조비교,반박전、반박중기화반박결속시고지사양조화고지사양+체외반박조혈청Chol화LDL명현승고(균P＜0.05).3조P'화지질과양화수평재분조사양전무현저차이(P＞0.05);반박전、반박중기화반박결속시,고지사양조여고지사양+체외반박조P'화지질과양화수평교정상사양조동시기균유현저증고(균P＜0.05);반박중기화반박결속시고지사양+체외반박조P'화지질과양화수평교고지사양조현저강저[P':(0.451±0.047)비(0.655±0.034),(0.561±0.043)비(0.723±0.050);지질과양화수평:(0.56±0.06)mmol/L비(0.88±0.07)mmol/L,(0.72±0.13)mmol/L비(1.23±0.11)mmol/L,균P＜0.05].결론 증강형체외반박가능통과감소지질과양화,개선혈소판막류동성조알고담고순혈증적병리생리진정,저가능시기발휘항동맥죽양경화적궤제지일.
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.