Abstract
Inflammatory response is an important determining factor for the mortality of patients with pulmonary thromboembolism. Inflammatory mediators can promote thrombus formation and increase hemodynamic instability. Urokinase is a commonly used drug for the treatment of PTE. The effect of urokinase on inflammatory reaction in PTE is still unclear. Our study was aimed at evaluating the effects of the intervention of urokinase and urokinase combined with aspirin in PTE rats. Results revealed that a large amount of infiltrated inflammatory cells surrounding the bronchus, vessels, and pulmonary mesenchyme, and even pulmonary abscess were observed in the PTE rats. CX3CL1/CX3CR1 coexpression, CX3CL1/NF-κB coexpression, and TXA2 were significantly higher. After treatment with urokinase, pulmonary embolism was partially dissolved and inflammatory cell infiltration was significantly reduced. The expression of TNNI3, BNP, D2D, PASP, PADP, PAMP, and TXA2, as well as CX3CL1/CX3CR1 coexpression and CX3CL1/NF-κB coexpression were significantly lowered. Aspirin showed no synergistic action. Therefore, these findings suggested the occurrence of inflammation during the process of PTE in rats. Urokinase treatment reduced the inflammatory response.
Highlights
Acute pulmonary embolism (PTE) leads to a rapid hemodynamic collapse and death
We found that lipopolysaccharide(LPS-) extracellular signal-regulated protein kinase (ERK), nuclear factor-κB (NF-κB), and CX3CL1 signal pathways exist in human bronchial epithelial cells [14]
The Inflammatory Response Existed in the Acute pulmonary embolism chronic thromboembolic pulmonary hypertension (CTEPH) (PTE) Process and Was Associated with NF-κB Pathway and CX3CL1/
Summary
Acute pulmonary embolism (PTE) leads to a rapid hemodynamic collapse and death. It is potentially a life-threatening disease with significant morbidity and fatal outcomes [1]. As a result of pulmonary hypertension, hemodynamically unstable patients are at high risk of death from worsening RV failure and cardiogenic shock, with a hospital mortality rate of >15% [2]. One quarter of the hemodynamically stable patients with PTE show the imaging or biomarker evidence of RV dilatation or dysfunction, with mortality rates ranging from 3% to 15% [3]. Inflammatory response is an important determining factor for the mortality of patients with pulmonary embolism. Leukocytosis and SIRS are important factors for determining the short-term outcomes in PTE patients clinically [4, 5]
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