Study On The Dependablity Between TM, APCR And Cerebral Infarction

Cerebral vascular disease(CVD) refers to brain dysfunction caused by a variety of cerebral vascular lesions.CVD or stroke in the narrow sense(Stroke), refers to the acute onset vascular case of the limitations or diffuse signs of brain function defect.Its high incidence,high mortality,high morbidity of stroke constitutes a huge threat to human health.Acute cerebrovascular disease(ACVD) incidence was higher trend,and tend to have younger because of dietary changes in the structure and the aging of society,this causes an immense burden on family and society.The risk factors of ischemic cerebrovascular disease(CVD) including atherosclerosis,hypertension,cardiac disease,diabetes,hyperlipemia,smoking and excessive drinking are generally acknowledged in the world.Virchow noted that the vessel wall injury,blood flow changes,blood changes in the nature are of the three elements of thrombosis formation,and prethrombotic state refers to the body imbalance of the procoagulant and natural anticoagulant mechanism, that is,vascular endothelial cells,platelets,coagulation and fibrinolytic system caused by changes in favor of thrombosis pathological status,are of the early stage of thrombosis formation.Protein C system(PCS) is a group of proteins, consist of protein C(PC),protein S(PS),protein C inhibitor(PCI),thrombomodulin (thrombomodulin,TM),plays an important regulatory role in blood coagulation of the body,is important in plasma anti-coagulation system,impacts the dynamic balance of blood coagulation - anticoagulant mechanisms directly, is related to the incidence of ischemic cerebrovascular disease closely.TM as one of the important components of PCS involved in anticoagulation effect.TM are single-chain glycoprotein,synthesized by vascular endothelial cells,together with the surface of endothelial cells.TM and thrombin 1:1 specific binding to change thrombin configuration,form thrombin-Tm complex.At the participation of Ca2+,bind specific to protein C,and activat it,to form thrombin-TM-protein C complex(APC).At the participation of protein S,APC inactivates factor V a and factorⅧa,at the same time inhibiting plasminogen activator inhibitor,to play the role of anticoagulation and promoting fibrinolysis.Combinating with TM,thrombin loss procoagulant activity,Including to prevent platelet aggregation release function,to prevent fibrin formation and activation of factorⅤand factorⅧ,which have important physiological significance in the prevention of thrombosis.TM have biphasic effect in the coagulation process. And activated protein C resistance(APCR) was mainly due to gene mutation of coagulation factorⅤ(ie,FV Leiden) and enable the activated protein C(APC) can not hydrolyzed and inactivated FⅤa,FⅧa effectively,making an increase of thrombin generation,resulting the hypercoagulable state in the body.In the normal population the incidence of APCR was also 5%,APCR-positive population may be considered high-risk groups of thrombosis.Therefore,the relations of TM,APCR and cerebral infarction were studied systematically to detect the relationship of TM,APCR with cerebral infarction and other stroke risk factors,which can provide a meaningful theoretical basis for prevention and treatment of stroke.Experimental Methods:select 60 cases of patients with acute cerebral infarction,one of 30 cases of male,female 30 cases,age 28-82 years old,the average age of 54.31±13.85 years old.Consistent with the diagnostic criteria that be revised by 1995 Fourth National Conference on Cerebrovascular Diseases,with the head CT or MRI confirmed,and by TCD(transcranial color Doppler ultrasound) and neck CDFI(neck color Doppler ultrasound) confirmed the exception of blood vessels narrow and harden.Selected 33 cases of healthy persons as a normal control group,one of 17 cases of male,female 16 cases,age 27-78 years old,the average age of 53.70±15.96 years old,and match the experimental group(P＞0.05).All patients except for acute and chronic liver disease,blood system disea,es,recent surgery,nephrotic syndrome and oral contraceptives,such as.Subjects were draw 3.6ml fasting blood into 0.4ml anticoagulant test tube containing 0.109mmol/L sodium citrate,3000r/min centrifugal 10min,check the upper plasma 1000μl,placed in-70℃refrigerator to be preserved seized.Using enzyme-linked immunosorbent assay method (ELISA) for plasma TM assay,sing APTT±APC(Dahlback) measured APCR.Experimental Results:There was significant differences between Plasma TM concentration(2.82±1.62) and the control group plasma TM concentrations (0.85±0.47),there was statistical significance.Under the modified Edinburgh-candinavian Stroke degree of neurological deficit score(MESSS) is divided into light,medium and heavy cerebral infarction.Inter-group comparison of plasma concentration of TM:The differences has statistical significance between light plasma TM concentration(1.71±0.71),medium-sized group of plasma TM concentration(2.94±0.85) and severe group of plasma TM concentration(4.94±1.46).There is significant difference,and there is statistical significance between experimental group,plasma APCR positive 12(20%) people and the control group plasma APCR positive one person(3.0%).There is significant difference and statistical significance between Youth Group plasma APCR positive rate (33.3%) and middle-aged and old groups of plasma APCR positive rate(11.1%); At the same time,the correlation analysis between plasmaTM concentration and risk factors of cerebral infarction show that there was positively correlated between.plasma TM concentration and systolic blood pressure,diastolic blood pressure,fasting blood glucose,cholesterol,triglycerides,LDL.There was negative correlation between plasma TM concentration and high density lipoprotein.Experimental conclusions:1.TM is a risk factor for cerebral infarction,there was positive correlation between TM and the severity of the cerebral infarction,TM increased on ischemic brain tissue has a protective effect.2.APCR was also one of the risk factors of high incidence of cerebral infarction,and have closer relationship with the incidence of youth stroke.3.The lower level of TM can produce acquired APCR phenomenon, thereby causing coagulation dysfunction,resulting in the occurrence of cerebral infarction.