Effect Of Huayu Jiedu Decoction On Expression Of D - Dimer, Endothelin - 1 And B - Type Brain Natriuretic Peptide In Rabbits With Acute Pulmonary Thromboembolism

Objective:The research heritage the Professor of Wang Jinda "bacteria, toxic, inflammatory" and rule on behalf of party "Xuebijing injection" medication, To " HuaYuJieDuFa " as the differential treatment principle. Through the femoral vein catheter for rabbits autologous thromboembolism, built the model of acute pulmonary thromboembolism. Based on the success of the model, given a certain dose Xuebi jing injection, Observed the effects of the Xuebijing injection for levels of D-dimer (D-dimer, DD), endothelin-1(Endothelin-1ET-1), sodium B-type brain natriuretic peptide (B-type natriuretic peptide BNP) changed and the intervention and its possible mechanism to APTE on plasma at different time points. Explord the Chinese medicine treatment of "Hua Yu Jie Du Fa",dialectical thinking and mechanism to APTE. Provided a theoretical basis and guidanced in the application of APTE for the "HuaYuJieDuFa".Method:Selection the New Zealand white rabbits32, male or female, weight:2.7±0.5kg/only; All the animals were fasted for12hours before the experiment, The use of randomly grouping number, were randomly divided into control group, model control group, Low molecular weight heparin group and Xuebijing groups, with8in each group. Reinfusion of autologous blood clots (Autologous blood clots through femoral vein catheterization), built the model of acute pulmonary thromboembolism. By the enzyme-linked immunosorbent assay, respectively, eight hours, one day, three days, five days, seven days after embolization, each time period, the levels of DD, ET-land BNP changed in plasma, seven days after all the excess rabbits were sacrificed, along drawn perpendicular to the direction of pulmonary, quickly remove the more serious lesions visually observed the lung tissue was placed in10%neutral formal in solution for24hours, embedded in paraffin, producer, HE staining of lung tissue, the lung tissue were observed under an optical microscope changes; Simultaneously taken out by the same method into the portion of the lung tissue, glutaraldehyde solution placed-5℃cryogenic refrigerator for24hours quickly, conventional dehydration, infiltration, embedding, polymeric, slicedand stained transmission, observed the changes of lung tissue under the electron microscope ultrastructural.Results:1. Each group ELISA assay (ELISA) test results showed: Control group:Five time points the levels of DD, ET-1and BNP were changed little compared before and after the group, the difference was not statistically significant (P>0.05); Model control group:The low molecular weight heparin group and Xuebijing group compared with the control group8hours after embolization, the levels of DD, ET-1and BNP were significantly increased, and the difference was statistically significant (P<0.05), and from the start of the first day after embolisming, gradually increased to three days after BNP levels begin to decline gradually to reach a peak, the7th days to a minimum value, but still more higher than the control group, the difference was statistically significant (P<0.05); The levels of ET-1continued to rise from the after embolization, could be decreased to5days, the difference was statistically significant (P<0.05); The levels of DD continued to rise to7days yet to see a downward trend, the difference was statistically significant (P<0.05). Xuebijing intervention group:The compared with the control group after embolization for8hours, the levels of DD, ET-1and BNP were significantly increased, the difference was statistically significant (P<0.05); Until the three days, The levels of DD and BNP would begin to decline after the peak, and ET-1began to decline to reach a Peak after embolization for five days, the difference was statistically significant (P<0.05); The levels of DD, ET-1and BNP were droped to near blank group, after the embolism for7days, but the difference was statistically significant (P<0.05). Low molecular weight heparin group: Compared with the control group, the levels of DD, ET-1and BNP were significantly increased, after embolization for8hours, the difference was statistically significant (P<0.05); The levels of DD, BNP began to rise to three days, the leves of ET-1began to decline after reaching a peak, after five days, the difference was statistically significant(P<0.05); Compared with the control group after the embolism for7days, the low molecular weight heparin in the intervention group,the level of DD, ET-1and BNP droped closer with the control group, the difference was statistically significant (P<0.05).2.HE staining of lung histopathology showed:Eye view: Control group:The lung tissue surface was smooth, pink, no bleeding, thrombosis and infarction. Model control group:the uneven surface of lung tissue, edema, atelectasis of lung tissue, many scattered bleeding points and shriveled necrosis, lung basal segments showed obvious necrosis of lung tissue, the surface was dark black. Low molecular weight heparin in the intervention group and Xuebijing intervention group:The lung tissue surface scattered bleeding, palered, structural integrity, mild swelling of lung tissue insufficiency, edema, lung embolism infarction bottom visible scar lesions. Endoscopic view:Control group:Alveolar size, uniform, visible capillaries rich, the structural integrity of the vessel wall, and no alveolar and pulmonary interstitial infiltration of inflammatory cells; Model control group:Lung tissues:Including alveolar epithelium, interstitial lung, blood vessels visible a large area of necrosis, interstitial pulmonary edema, exudate, and outline the basic structure of the lung tissue disappeared, showing a large thrombus attached to the inside of blood vessels, which saw a large number of inflammatory cells(lymphocytes and neutrophils) and colony infiltration; Low molecular heparin intervention group:Most lung tissue necrosis, alveolar edema, some contours remain, part of the structure is unclear (necrosis longer), which saw more inflammatory cell infiltration, could be seen within the pulmonary artery thrombosis; Xuebijing intervention group:The pulmonary emboli still visibled within and small pieces of lung tissue necrosis, organizational structure and outline of surviving, some tissue cell death, seen in a small amount of inflammatory cell infiltration.3. Ultrastructure of lung tissue showed: Control group:The structure of capillary endothelial cells, basement membrane integrity, visible red blood cells in the lumen, structural integrity deformities, lung tissue blood barrier clear, complete mitochondrial structure, the type of Ⅰ and Ⅱ epithelial edema, alveolar epithelial clear. Model group:Lung tissue basement membrane rupture, vascular endothelial cells, alveolar the type of Ⅰ and Ⅱ epithelial cells structure was unclear, cell surface microvilli disappeared, concentrated cytoplasm and nucleus chromatin condensation, saw a lot of cleavage fission fragments formed after shedding apoptotic bodies, mitochondrial structural damage. Low molecular weight heparin group:Capillary endothelial cell swelling, necrosis seen in a lot of oozing blood cells, blocking the lumen; Loose the type of Ⅱ epithelial cells, edema, most lamellar bodies vacuoles. Xuebijing intervention groups:Mild swelling of capillary endothelial cells, intraluminal necrotic oozing blood cells, blocking the lumen, the link was normal; The type of Ⅱepithelial cell edma, lamellar bodies emptying reduced.Conclusion:Xuebijing injection could significantly reduce the levels of DD, ET-1, BNP of plasma, in the pulmonary embolism with rabbit, improved pulmonary coagulation and fibrinolysis system, reducing endothelial cell damage, reduced pulmonary capillary pressure and improve right ventricular dysfunction; Pathological studies of lung tissue Show: Xuebi jing injection reduced pulmonary thromboembolism rabbit lung tissue inflammatory infiltration, reduced infarct size; Lung tissue ultrastructure showed:Xuebijing injection protected the lung tissue of rabbit vascular endothelial cells, alveolar the type of Ⅰ、Ⅱ cells ventilatory dysfunction epithelial cell damage, improved pulmonary thromboembolism after pulmonary embolism.