Correlation Of VWF Active Ation In Reperfusion Of No Reflow Phenomenon After Acute Myocardial Infarction In Mice

Background By the living standards improve,atherosclerotic disease has become the number one killer that seriously affects people’s living standards The incidence of coronary heart disease is increasing year by year.Acute myocardial infarction(AMI),as a common acute critical disease,seriously endangers human health.Eemergency having Pereutaneous Coronary Intervention(PCI)is one of the most important reperfusion therapy for the treatment of AMI.In recent years,through the reperfusion therapy,the rate of successful taking criminal vascular is graduated increase,so that criminals patency rate increased year by year,the success of the emergency PCI after 5%-50% of the patients with epicardial coronary artery perfusion is good,but there are still poor myocardial perfusion in 13%-40% patients with No Reflow(NR)or slow flow phenomenon.NR is one of the serious complications of AMI reperfusion therapy.In recent years,it is one of the urgent problems to improve the microcirculation and restore the function of the myocardium by reperfusion therapy.At present,pathogenesis progess of NR is unclear,the possible mechanism for the complex flow and tissue factor and tissue factor pathway inhibitor imbalance lead to vascular endothelial cells and the ischemic injury of myocardial cells,blood coagulation disorder and anticoagulant mechanism,microthrombosis,microvascular spasm and obstruction,neutrophil aggregation and the release of oxygen free radicals and inflamemation factor release guide antiinflammatory with the proinflammatory disorder,inflammatory reaction further produce further cascade amplification reaction,such as the result of the interaction.The vascular endothelial cell dysfunction and damage plays an important role in NR occur.Von Willebrand Factor(vWF)was synthesized from within the vascular endothelial cells and megakaryocyte which has the function of adhesion of a kind of glycoll lprotein,mainly exist in the endothelial cells Wellel-Palade release in the circulateon of the blood corpuscle,hemostatic effect of glycoprotein.vWF mechanism may be involved in acute myocardial infarction reperfusion NR phenomenon of mechanism is: when endothelial damage,vWF release in endothelial cells into the bloodstream,mediated adhesion,platelet and subcutaneous collagen fibers within activated platelets,stimulate hyperplasia of smooth muscle cells in essel walls,andfurther vascular luminal stenosis.When endothelial cell damage,vWF can quickly attached to the damaged blood vessels within the skin,as a carrier protein Ⅷ:C and play a role,become an important factor to promote thrombosis,thus increasing AMI after reperfusion the occurrence of NR.Therefore,this paper discusses the mechanism of vWF affect NR after AMI reperfusion is particularly important.Objectives:1.Toexplor the non-invasive trachea intubation through oral for AMI after reperfusion in mice model of NR method is reliable or not.2.To investigate the vWF in mice with AMI after reperfusion NR mRNA and protein levels.Methods:1.Select 56 wild mice as the research object,12 in normal group,Sham group and NR group both have 22 wild mouse;Seleced 10 mice in Sham group and NR group,through 30 min reperfusion after 30 min after AMI.Intraoperative record ECG findings in mice;Postoperative line of Evans blue-Triphenyltetrazolium chloride(TTC)staining confirmed ischemia and myocardial infarction area;Line of thioflavine S staining confirmed that NR model building a successful and recorded in the common parts NR.On the basis of the successful build model take mice to check the other vWF reperfusion of NR effects.2.Using immunohistochemical staining method detection in normal group,Sham group,NR group in above NR parts,no reflow parts,below NR vWF expression in the following sections.3.Western blot to cheak the vWF protein expression in NR parts.4.Quantitative real time RT-PCR to detect the vWF corresponding mRNA expression in NR parts.Results:1.For Evans blue-TTC staining and by recording the electrocardiogram showed ischemia and myocardial infarction models were prepared successfully;for thioflavine S staining confirmed myocardial infarction reperfusion in mice NR model was successfully established;NR position on the anterior wall of the left ventricle in 1-3mm below the ligature,canterior descending territory.2.Immunohistochemical staining showed NR above the area of the normal group was increased,the difference was statistically significant(P<0.001);NR group compared with Sham expression increase,the difference was statistically significant(P<0.05)(Figure 6);group NR positive staining was found after analyzing the visible parts of the imageL: NR group compared with normal group and Sham group of regional vWF expression increased,vWF expression in Sham group than in normal group increased;the difference was statistically significant(P<0.05)(Figure 7);for the NR region below the positive staining image analysis of the expression of vWF: Sham group compared with normal group and NR group increased.No statistically significant differences(P>0.05).3.The expression of vWF at the NR site mRNA: the mRNA expression of vWF in the NR group was significantly increased in the NR group compared with the group normal and the Sham group,and the difference was not statistically significant.4.The expression of vWF in NR site protein level: the expression of vWF protein in the NR site of NR group was significantly increased compared with group normal and Sham group,and the difference was statistically significant increase of AMI after reperfusion NR.Conclusions:1.Non-invasive trachea intubation through orafor acute myocardial infarction after reperfusion in mice model of no reflow method is reliable.2.After AMI reperfusion NR phenomenon in the process of vascular endothelial cell injury,activation of the inflammatory response,microcirculation obstacles to work increase the expression of vWF,there by affecting the damage of vascular endothelial cells can promote thrombus formation,increase microcirculation dysfunction,and increased AMI after reperfusion injury.At the same time,how to effectively inhibit the expression of vWF after AMI reperfusion therapy may be a new target for the treatment of NR.