| Background and objective: Acute pulmonary embolism (APE) is a very common disease with high morbidity and mortality in clinical practice. Improving the lysis of thrombi in patients with pulmonary embolism remains a challenge. Unfortunately, there are some emboli which can not be lysised completely even under anticoagulation and thrombolytic therapy. Clinical and experimental studies suggest that pulmonary emboli resist endogenous fibrinolysis and lysis induced by plasminogen activator. This resistance to lysis is due in part to specific molecular factors in the thrombus to oppose fibrinolysis. Hence, foundamental insights into the molecular factors that oppose physiological or pharmacological lysis in thrombi will be necessary to improve treatments for pulmonary embolism. Present paper speculates that the lysis of thrombi can also be affected by endogenous coagulation and fibrinolysis system in local circumstances of thromboembolic pulmonary artery after pulmonary embolism. So we analysis the level of some gene expression involving coagulation factor(tissue factor and tissue factor pathway inhibitor) and fibrinolysis factor(tissue plasminogen activator and plasminogen activator inhibitor-I) in the local thromboembolic and non-thromboembolic pulmonary artery in APE rabbit, to find out which factors maybe affect the lysis of emboli in the lung.Methods: Anesthetized 34 rabbits received autologous clots througe jugular vein to establish the pulmonary embolism model. They were divided into groups as follows: APE 3hs, PE 8hs, and PE 24hs group and their corresponding control groups. Thromboembolic, non thromboembolic and normal pulmonary artery were obtained from all groups rabbits. Heart, aorta, liver and adipose tissues alsoobtained from rabbits. All tissues were examined to quantify the amount of TF, TFPI, PAI-1 mRNA expression by RT-PCR method. And also analyzed the expression of PAI-1 and t-PA protein in pulmonary and aortic arteries using immunohistochemical method.Experiment 1. Establishment of rabbit acute pulmonary embolism model Rusults: 1. The successful rate of APE model was 87.18%, 5 of them were died. 2.About 3-5 emboli could be found in the lung of each rabbit, most of them occluded in segment of PA. After APE 3hs and 8hs, the emboli almost remain integrated in the pulmonary artery. While after APE 24 hs, part of emboli had been lysised incompletely, and some of them were put into the distal of pulmonary artery. Conclusion: The successful rate on establishment of APE, which can provide a good model for basic APE study.Experiment 2. Assessment of infrastructure of pulmonary artery in acute pulmonary embolism rabbitResults: 1. APE 3hs group, part of endothelial cell were denudated: smooth muscle cells(SMCs) showed synthesis phenotype, and migrated to endothelium; some protein coagulated beness endothelium; and lymphocyte was activated. 2. APE 8hs group, some of endothelial cell were denudated; subendothelium edema, and fluid pressure was high; large amount of protein were coagulated ; some of SMCs existed para-apoptosis; SMCs in the shallow layer were synthesis phenotype. while in deep layer. SMCs were systolic phenotype. 3. APE 24hs group, a large amount of endothelial cell were denudated; SMCs were migrated to naked faces of endothelium denudated; subendothelium edema, local fluid pressure increased; lymphocyte was activated; and mast cells were also activated. Conclusion: After APE. the local thromboembolic PA were damaged, the tissue and structure also changed, some of cell such as lymphocyte and mast cell were activited. some cytokine secreated from activited cells may affect the coagulationand fibrinolysis in local lesion pulmonary artery.Experiment 3. Expression of tissue factor mRNA in tissues of acute pulmonary embolism rabbitResults: l.APE 3hs and 8hs groups, the level of TF mRNA expression in thromboembolic PA was significantly higher than that of non-thromboembolic PA and normal PA, in 3hs group , they were 1.10±0.21, 0.40±0.29, 0.84±0.26, respective...
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