Study On Dynamic Variation Of Thrombomodulin In Patients With Cerebral Hemorrhage

Background: Thrombomodulin(TM) is a monochain glucoprotein exists on endothelial cell membrane. TM is synthesized by vascular endotheliocyte and placental trophocyte. Its gene locates in chromosomes of number 20. E-smon etal found it in 1981, and then separated this active mass successfully at 1982 and named it thrombomodulin. From then on, people found out that TM distributed diffusely on endothelia of arteries, veins, capillary vessels and lymphatics, especially on that of tissues of lung, kidney and placenta. TM play a important role in blood anticoagulant mechanism.It can make anticoagulant and fibrinolyticative functions throught acceleration thrombase activing protein C and make direct anticoagulant effect through inhibitory thrombases activation. Because TM is specific distribution on vascular endothelia, so it can become a molecular sign of vessel wall lesions and angioma. It offers a new way in clinic on measurement of PC activation, diagnosis and therapy of thrombosis, diagnosis of angioma and early monitoring vessel wall lesion. After study on TM change in cerebral vascular diseases, people found out that TM as a sign of endothelial lesions, would rise significantly no matter in cerebral infarction or cerebral hemorrhage, in acute stage or restoration stage, but dymanic observation on TM in different periods of cerebral hemorrhage still haven't been done and meaning of TM's dynamic variation in cerebral hemorrhage remains unknown. So my study is on dynamic variation of TM in cerebral hemorrhage. Objective:To observe the dynamic variation of thrombomodulin in different periods of patients with cerebral hemorrhage, and to probe the change of vascular endothelial lesion in different periods of cerebral hemorrhage and the effect of blood coagulation mechanism.Methods :The thrombomodulin levels of 53cases cerebral hemorrhages were mearsured respectively at 1~3d and 10~14d in 25 cases and only at 1~ 3d in another 28 cases by means of ELISA.Results:Levels of TM in 25 patients with cerebral hemorrhage 1 -—3d were lower than those of 10~14d. Levels of TM in another 28 patients group were higher than previous group those of 10~14d and 1~3d. Levels of all 1-3d(53cases) were lower than those of 10~14d. But all of these differences have no statistical significance.Conclusion:Levels of TM in patients with cerebral hemorrhage have no significant variety between those of 1 — 3d and 10 — 14d. Endothelial damage caused by cerebral hemorrhage continues on more than 10~14d. Continuous high level of TM has anticoagulant activation, is an independent risk factor of cerebral hemorrhage.