| Objective:Pulmonary thromboembolism (PTE) is a serious disease caused by the thrombus from the venous system or right heart which obstruct the pulmonary artery or its branches, its main clinical and pathophysiological features is pulmonary circulation and respiratory dysfunction. At present, the pathophysiology of PTE on molecular and cellular level is still unclear, most scholars believed that the pathological process of pulmonary embolism is associated with inflammation. Recently some literature reported that the immunology response may associate with pulmonary artery reconstruction, but still lack the experimental evidence. Our study assumes pulmonary artery reconstruction is associated with inflammation, cytokines and former fibrosis chemokines.IL-13 is a kind of cytokines that drives from different T cell and dendritic cell, mainly by Th2 cells. A recent report confirmed that IL-13 system is a new type of pulmonary artery smooth muscle cell growth regulation system.IL-13 can induce the production of potential TGF-β, indirect active TGF-B, hypoxia could also lead the increase expression of TGF-B. TGF-B is a kind of important factor which regulation the proliferation and differentiation of cells, it can also promote the proliferation of vascular smooth muscle cell, and is associate with a variety of cardiovascular diseases.Our subject will build the APE animal model, anlysis its pathobiology, and discuses the association between IL-13, TGF-B and pulmonary hypertension.Methods:The study was divided into three parts.In the first part: 36 rabbits were randomly divided into acute pulmonary embolism group and control group. We transfused the antilogous blood clots to establish PTE model, the control group were given equal amount of 0.9% sodium chloride solution. Then digital subtraction angiography was used to determine whether the model is success.In the second part: We collect the pulmonary artery and its surrounding tissue at 48h,4d,14d. HE staining and Masson staining were used for histological analysis.In the third part: collected serum at 48h,4d,14d, use enzyme-linked immunity assay (ELISA) detect the lever of IL-13, TGF-β.Statistical software SPSS 13.0 was used for statistical analysis, data described as mean±standard. analysis of variance (One-Way ANOVA) was used to assay the data at different time points, t test (t-test analysis) was used to assay the data of each group, pearson analysis was used to assay the correlation between the data, P<0.05 was considered statistically significant.Results:The first part:In this 22 rabits, we successful made18 PTE model. One died of anesthetic accident, three died of extensive thrombosis. Success rate was 81.8%. Most APE were happened on the level of lung segment. RR, HR, AaD02 were increase in the early stage of pulmonary embolism.The second part: Neutrophil increased in affected pulmonary artery wall on day 4, and also increased in distal pulmonary artery on day 2, (P<0.05). The analysis also show that the endomembrane was more thick on day 14 than before (P<0.05).The third part: The serum level of IL-13, TGF-βis 36.86±3.06pg/mg,1591.67±55.01pg/mg, significant increase on day 4 and day 14, respectively.Conclusion:1. Reinfusion of autologous blood clots to establish acute pulmonary thromboembolism is with a high success rate. Distribution of the emboli is similar to clinical distribution. AaDO2 can be used as indicators of early diagnosis of pulmonary embolism. RR and HR immediately increase after pulmonary embolism, the recovery of HR before RR.2. Inflammatory cell infiltration is not only appear in the pulmonary artery wall, but also in substance.Alveolar septum can be seen neutrophil infiltration,we also can see atelectasis.The pathological of PTE maybe associated with inflammatory cell infiltration.3. Th2 type immune response may partly play a role in PE, IL-13 and TGF-βmay interact to promote collagen production and lead fibrosis, partly involved in pulmonary artery reconstruction. However, there is no correlation between two indicators. |
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