血小板活化及内皮细胞在原位肺动脉血栓形成中作用机制的研究进展  

Research Progress in the Mechanism of Platelet Activation and Endothelial Cells in In Situ Pulmonary Artery Thrombosis

作　　者：许小艳 李桂琼[2] 

机构地区：[1]重庆医科大学,重庆 [2]重庆医科大学附属第二医院,重庆

出　　处：《临床医学进展》2021年第12期5747-5753,共7页Advances in Clinical Medicine

摘　　要：普遍认为,肺栓塞是由静脉血栓脱落,随血流进入肺动脉造成梗死。这一概念在临床实践中持续了一个多世纪。但随着越来越多的检查技术的出现,发现了在许多情况下,越来越多的肺栓塞找不到明显的栓子来源。包括慢性阻塞性肺疾病、哮喘、急诊/择期手术、病毒性肺炎等,上述疾病都有发现肺栓塞的形成,却未发现深静脉血栓。对于原位肺动脉血栓形成的过程,经过实验及临床观察证明,内皮细胞及血小板活化起了关键性作用。内皮功能障碍、缺氧、炎症细胞因子、基因突变等均是原位肺动脉血栓形成的基础。这篇综述将会讨论原位肺动脉血栓形成的潜在机制。It is generally believed that the pulmonary embolism is from venous thrombosis, and the blood flow is formed into pulmonary artery. This concept lasted for more than a century in clinical practice. However, with more and more inspection techniques, the embolus is not found in many pulmonary embolism cases, including chronic obstructive pulmonary disease, asthma, emergency/alternative surgery, viral pneumonia, etc. The above diseases have foundation of pulmonary embolism without deep vein thrombosis. After experimentation and clinical observation, endothelial cells and platelet activation plays a key role in the formation of in situ pulmonary artery thrombosis. Endothelial dysfunction, hypoxia, inflammatory cytokine, gene mutation, etc. are the foundations of in situ pulmonary artery thrombosis. This review will discuss the potential mechanism of the in situ pulmonary artery thrombosis.

关 键 词：肺栓塞 原位肺动脉血栓形成 内皮细胞 血小板活化 

分 类 号：R56[医药卫生—呼吸系统]