The Determination And Clinical Significance Of Plasma Fibronectin And Platelet Parameters In Cerebral Infarction Patients

Cerebral infarction(CI) is the most common type of cerebral vascular diseases,nearly accounts for 75%. The incidence of CI holds young potential recently,which gives rise to enormous damages to the society as well as the families. Cerebral thrombosis is the most common reason of cerebral infarction.Platelet is one of the tangible elements in blood,the quantity of platelet influences the blood viscosity directly,the hyper-function of it leads to hypercoagulable state in blood,which is a critical factor of thrombosis.The three parameters of platelet—platelet count(PLT),mean platelet volume(MPV)and platelet distribution width(PDW)—are the important hema-cytologic indexes which can reflect the function of platelet.Recent study demonstrated that Fibronectin(Fn) probably participates in platelet adherence and aggregation and is an important protein ligand within the thrombosis.Though it is important to approach pathogenesy and prevention and therapy of CI by approaching the variation regularity of above-mentioned parameters,there is no consistent conclusion about the variation of PLT,MPV,PDW and Fn at different periods or in different infarction sizes.The study selectes from the CI patients(CI group) who registered fromMarch of 2005 to March of 2006 in the department of Neurology of the second hospital in Jilin University and from the healthy physical examinees(control group) in the physical examination center in the same hospital and during the same interval.With regard to platelet study group:580 CI patients in experimental group,397 healthy examinees in control; plasma Fn study group:493 in experimental group,349 in control.In addition,in terms of time of incidence(in 48h,49h-7d,8-14d and after 14d)and infarct size(large size,small size and lacunar CI),we separate the CI group into different subgroups,compare each subgroup with control separately,and also make group comparison between platelet group and Fn group,in order to approach the regularity and significance of the variations of the above-mentioned indexs.The results show that: The PLT is the lowest in 48h after CI onset, but ascend gradually with the time developed,and recovered to normal level at the 14 days post-currently(P<0.05).The reason may be that there are large quantities of platelets be consumed and destroyed before onset and acute stage of post onset,which stimulate the marrow-megakaryocytes respond actively and generate new platelets compensatively, which leads PLT recovered to normal level gradually.Versus control group,MPV and PDW ascend markedly in 48h after CI onset(P<0.05),and reach the peaks at the time of 48h-7d,then descend gradually,but even higher than control group at the recovery period(P<0.05).That demonstrates that the morphologic variation happended before stroke.Martin and companions discovered that MPV of the patients with cerebral arteriosclerosis has increased before CI occured.There are plenty of neoformative large volume platelets in peripheral blood,and also small volume platelets remained simultaneously,that causes PDW ascent followed with MPV ascent. The larger the platelet is,the more granules it contains,the more activate substantials it releases,and also more contributions to platelet adhesion and aggregation reaction,which leads to cerebral infarction developed further.During the process of CI,PLT descends significantly,in order to maintain the constancy of thrombocytocrit(PCT),so MPV ascends further more.With the condition of the CI patients improves,PLT recovers gradually,so MPV descends.But the pathological change of artherosclerosis still existing,which causes MPV of the CI reconvalescents still be higher than the control group.Due to the positive correlation between PDW and MPV,the variation regularity of PDW keep coincidence with MPV at all periods of cerebral infarction.Versus control group,plasma Fn ascend markedly in 48h after CI onset(P<0.05), then present descending tendency gradually,plasma Fn is even markedly higher than control group at the 14 days post-currently(P<0.05).That may be there are quantity of platelet activation after CI onset,Fn in platelets be released to plasma withα-granules;otherwise, vascular endothelial cells which injured at acute stage of cerebral infarction secrete more Fn;atherosclerotic plaques which contain plenty of Fn be destroyed and release fraction of Fn into blood,lead to content of Fn ascend in circulation blood.In addition,as non-specific opsonin,Fn is able to maintain the dynamic balance of coagulo-plasmino system,possesses the function of antithrombotic. The patients who are at the acute stage of CI in hypercoagulabale state,because of physical stress synthesize and secrete more Fn compensatively,which cause plasma Fn ascent further more. With the patients condition improves,platelets destruction decreased, endangium injury relieved,so Fn released to blood decreased,which provoke plasma descend gradually.Till the CI recovery period,the patients still have artherosclerosis,which can give rise to recurrence of CI easily, so the plasma Fn in patients still markedly higher compare to control group due to the function of Fn—maintain the dynamic balance of coagulo-plasino system(P<0.05).It is evident that because of the hyper-functional platelets in the CI liability populations and CI patients,the platelets are prone to adhere and aggregate,so clinically use anti-platelet drugs amid the above-mentioned crowd in the early stage plays a significant role in CI prevetion and therapy.Fn can initiate CI and anti-thrombosis as well.At present,there has no definite conclusion about to which level should we adjust the plasma Fn in CI is benefit to the patients,so the therapy of plasma Fn adjustment has not emerged.The larger the infarct size is,the lower the PLT is,and the higher the MPV,PDW and plasma Fn are;However,compare with control,PLT in Lacunar CI patients has no significant difference(P>0.05).There are large quantities of platelet consumed during the process of thrombosis, result in PLT in peripheral blood descending,that provoke the infarct size larger,and stimulating the marrow-megakaryocytes proliferate stronger compensatively,so cause MPV and PDW ascending markedly.And the larger the platelet is,the more granules it contains,the more activate substantials it releases,and also more prone to platelet adhesion and aggregation reaction,which leads to the infarct size much larger.At present,the pathogenesis of Lacunar cerebral infarction may be the tube occlusion causedby the lipid hyaline degeneration of the small arteries and micro arteries,so this procedure has not much the platelet consumption,which may be the reason that comparing with the control group,the PLT in Lacunar CI group has no significant difference(P>0.05).The more platelet consumed in CI patients,the more severe endangium injured,the more Fn released to the blood,the larger infarction volume is.Furthermore, the larger infarction volume in CI patient is,the higher MPV is, the moreα-granules contains in the platelets,so when platelets activated,the more Fn that contained inα-granules released to the blood with granules,which also provoke plasma Fn ascent.Moreover,because of antithrombotic function of Fn, the larger infarction volume is, the more Fn the liver synthesize and secrete compensatively,that lead to plasma Fn ascent markedly.We can assess the CI patients'pathogenetic condition and prognosis roughly according to the platelet parameters and plasma Fn. The CI patient who has the lower PLT and the higher MPV and PDW,may suffer the larger infarct size,the condition may be more severe.Therapeutically,such patients should receive more dosage of anti-platelet drugs in the early stage,in order to improve prognosis and attain better therapeutic effects. Dynamic monitoringplatelet parameters and plasma Fn during the therapy may contribute doctors to master the patients'condition.