心肌缺血再灌注损伤大鼠血浆蛋白C活性变化及机制研究  

Research on the changes of protein C activity in plasma with myocardial ischemia reperfusion injury in rats and its mechanism

作　　者：张娅[1] 张根葆[1,2] 季娜[1] 王斐[1] 吴娟[1,2] 

机构地区：[1]皖南医学院病理生理学教研室 [2]皖南医学院蛇毒研究所安徽省重点实验室

出　　处：《中国临床药理学与治疗学》2015年第3期284-288,共5页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：安徽省教育厅自然科学研究基金重点项目(KJ2011A266);活性生物大分子研究安徽省重点实验室(科基[2012]126号)

摘　　要：目的:探讨大鼠心肌缺血再灌注损伤时血浆蛋白C(PC)活性变化及其可能机制。方法:SD雄性大鼠50只随机分成对照组(C)和缺血再灌组(IR),IR组按照缺血和再灌的时间分为缺血30min(I30)、再灌30min(R30)、60min(R60)和120min(R120)组,每组10只。通过结扎大鼠心脏左冠状动脉前降支30min后再灌注的方法制备在体IR模型,采用生物信号采集处理系统连续监测心电图变化。从颈总动脉取血,检测活化部分凝血活酶时间(APTT)、血浆凝血酶原时间(PT)、血浆凝血酶时间(TT);以发色底物法检测血浆PC活性;比浊法测定血小板聚集率;酶联免疫吸附法检测血浆游离蛋白S(FPS)的含量;光镜观察心肌组织学改变。结果:IR组大鼠心电图明显改变且病理观察显示心肌细胞排列紊乱、细胞核固缩、间质水肿;与C组比较,血浆PC活性I30组明显下降(P<0.01),再灌注初期回升,而R120再次下降(P<0.01);血浆FPS含量再灌注初期升高(P<0.05),R120下降(P<0.05);血小板聚集率I30组和再灌注初期(R30、R60)升高(P<0.01);APTT再灌60min后明显缩短(P<0.01),PT R120组缩短(P<0.01),TT无明显改变。结论:血浆PC活性在心肌缺血再灌注期间发生显著变化,其机制可能与血小板的活化及血浆FPS含量改变有关。AIM：To investigate the active change of plasma protein C（PC）,and its possible mechanism of myocardial ischemia-reperfusion injury in rats.METHODS：50SD male rats were randomly divided into control group（C）and ischemia reperfusion group（IR）,then the rats of ischemia reperfusion group were randomly divided into ischemia 30min（I30）,reperfusion30（R30）,60（R60）and 120（R120）min group with10 in each group.Ligated the rats＇ left anterior descending coronary artery 30 min then perfused to establish the model of ischemia reperfusion in vivo,monitored ECG changes in rat hart continuously by biological signal collection and processing system.Took carotid artery blood of the rats,to activated APTT,PT and TT;by chromomeric substrate method to tested PC activity;by enzyme linked immunosorbent assay（ELISA）to the content of Plasma free protein S（FPS）;by turbidimetry to platelet aggregation rate;by a microscope to observe myocardial cells and interstitial organization.RESULTS：The ECG of ischemia reperfusion rats changed significantly and pathological observation showed disordered arrangement of myocardial cells,the nucleus pycnosis,interstitial edema;compared with control group,the plasma protein C activity decreased significantly（P〈0.01）at ischemia30 min,evidently picked up at early reperfusion,decreased again（P〈0.01）at reperfusion120 min;the content of plasma FPS apparently elevated at reperfusion 30 and 60min（P〈0.05）,then was significantly down at reperfusion 120min（P〈0.05）;platelet aggregation rate increased significantly（P〈0.01）at ischemia 30 min,reperfusion 30 and 60min;APTT significantly shortened after reperfusion 60min（P〈0.01）.PT shortened after reperfusion120min（P〈0.01）,TT had not obviously change.CONCLUSION：The plasma protein C activity changed significantly during myocardial ischemia reperfusion and its mechanism may be related to the change of plasma FPS content and activation of platelets.

关 键 词：心肌 缺血再灌注损伤 蛋白C 血小板聚集率 蛋白S 

分 类 号：R965.2[医药卫生—药理学]