| Objectives:At present,cerebrovascular disease is a serious threat to human health,and its morbidity,mortality and disability rate are very high.Hemorrhagic cerebral apoplexy is our commonly known as the intracerebral hemorrhage.Its morbidity is lower than that of ischemic stroke,but it has a more rapid onset,faster disease progression,and higher mortality and disability rate.Hypertensive intracerebral hemorrhage is the most common,accounting for 70%-80% of all patients with cerebral hemorrhage.Although the pathological basis of HICH has not yet been clearly defined,Most researchers believe that the formation of HICH is mainly because of long-term hypertension lead to cerebral artery wall elasticity decreased and increased brittleness as well as the formation of atherosclerosis.After the occurrence of HICH,the occupying effect of hematoma can directly damage the brain tissue.Indirect effects,such as inflammatory factors infiltration,edema formation,intracranial hypertension and other factors can lead to further damage of brain tissue.Therefore,through the experiment on the occurrence of HICH further study,not only can we have a deeper understanding of the pathogenesis of HICH,but also can we be provided more help for the treatment of HICH with the clinical contact.In the study of the pathogenesis of HICH,we found that long-term hypertension on the arterial wall of the chronic damage,resulting in vascular endothelial cell damage and increased arterial fragility,which could lead to the occurrence of HICH.Vascular endothelial cells are the part of the blood-brain barrier.The injury of endothelial cells can directly increase the permeability of BBB and cause microcirculatory disturbance,which is an important factor for the aggravation of cerebral edema.Von Willebrand factor is a kind of glycoprotein produced by endothelial cells or megakaryocytes,which is involved in the process of coagulation and plaque formation,which is involved in the process of coagulation and atherosclerotic plaque formation.vWF in plasma mainly comes from endothelial cells.In the vascular endothelial cell damage,collagen is exposed,vWF's structure changes,the synthesis of vWF is increased and a large number of vWF released into the blood.The elevation of vWF reflects the damage of endothelial function,which is involved in the further damage of nerve cells.Studies have shown that vWF can be used as a marker of endothelial damage.CD40 is a transmembrane protein that is a member of the tumor necrosis factor receptor superfamily.CD40 L is a ligand,which plays an important role in signal transduction and plays an important role in the inflammatory response of AS through CD40/CD40 L interaction.CD40 and CD40 L are present in AS-related cell surfaces,Such as endothelial cells,macrophages,monocytes and so on.CD40 L is not expressed on the surface of resting platelets.But after platelet activation,the internal storage of CD40 L can be quickly transferred to the membrane,in a short period of time,CD40 L off through the hydrolysis of the protein,which is soluble CD40 L.SCD40L is a molecule associated with angiogenesis and inflammatory responses,.It induces the expression of proinflammatory cytokines,produces and releases proinflammatory mediators,integrins,and Matrix-metalloproteinases.It is involved in the injury of inflammatory cells,and can participate in the damage of blood vessels.We have studied the levels of vWF and sCD40 L in serum of HICH patients.We have understood the correlation between the two factors and the pathogenesis of HICH,and their correlation with the degree of neurological impairment,which provides more evidence.Method:(1)We have collected hospitalized HICH patients in 60 cases,set to cerebral hemorrhage group,and collected the onset time in 24 hours,1 week,2 weeks of venous blood.We have also collected outpatients with primary hypertension in 36 cases,set to control group,the same method to collect venous blood.(2)Serum levels of vWF and sCD40 L have be determined by ELISA.Comparing the relationship between the serum vWF and sCD40 L levels and the time of onset in patients with HICH.Comparing of serum levels of vWF and sCD40 L with bleeding site,bleeding volume,edema volume,and NIHSS score.(3)Using SPSSl9.0 statistical software for data processing,all the data in the form of meanąstandard deviation,the test level of P<0.05 that the difference is significant.Results:(1)The 60 patients with HICH in the hospital are named cerebral hemorrhage group.Gathering their onset time within 24 hours,1 week,and 2 weeks of venous blood.The 36 patients with primary hypertension are named control group.Gathering their current venous blood.(2)There is no correlation between serum vWF and sCD40 L in HICH patients(P>0.05).(3)The serum vWF level is positively correlated with the amount of bleeding volume(r=0.498,P<0.01),edema volume(r=0.512,P<0.01)and NIHSS score(r=0.858,P<0.01)in HICH patients.The serum sCD40 L level is positively correlated with the amount of bleeding volume(r=0.483,P<0.01),edema volume(r=0.479,P<0.01)and NIHSS score(r=0.178,P<0.01)in HICH patients as well.Conclusion:(1)Serum levels of vWF and s CD40 L are significantly elevated within 24 hours of onset of HICH.At the onset of 1 weeks,the level reaches the peak,and decreases at the onset of 2 weeks.But the level of the two factors are higher than the control group in each time period,which is consistent with the peak of brain edema.The results have showed that endothelial cell injury and inflammatory reaction persisted after HICH.(2)The levels of vWF and sCD40 L in serum are not related to the bleeding site of HICH patients,and there is a significant positive correlation with the volume of hemorrhage and edema.(3)The serum vWF and sCD40 L level is positively correlated with the NIHSS score.The results have showed that they are also directly proportional to the severity of neurological impairment.Early determination of their content can be combined with CT results to assist in the assessment of disease. |
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