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冠状动脉持续闭塞后,通过溶栓疗法、冠状动脉旁路移植术、经皮冠状动脉介入治疗等的建立和推广,使急性阻塞的冠状动脉多能及时再通,缺血的心肌重新获得血液供应。但是,再灌注之后可能使原有的心肌缺血性损伤进一步加重,即发生心肌缺血再灌注损伤。研究表明,微血管损伤是心肌缺血再灌注损伤的重要发病机制之一。激活的血管内皮细胞和白细胞相互作用,对血液流变学、微血管口径及血管通透性的影响即产生冠状动脉无复流现象。冠状动脉无复流与炎症反应相关。白细胞,一些炎症细胞因子如白细胞介素-6、白细胞介素-8、白细胞介素-10和肿瘤坏死因子-α等,均参与了冠状动脉无复流过程且发挥了重要作用。
After the continuous occlusion of the coronary artery, the establishment and promotion of thrombolytic therapy, coronary artery bypass grafting and percutaneous coronary intervention can make the acute obstructed coronary artery more timely and recanalized, and the ischemic myocardium regains blood supply . However, after reperfusion may make the original myocardial ischemic injury further aggravated, that is, myocardial ischemia-reperfusion injury occurs. Studies have shown that microvascular injury is one of the important pathogenesis of myocardial ischemia-reperfusion injury. Activated vascular endothelial cells and leukocytes interaction, the impact on hemorheology, microvascular caliber and vascular permeability that produces coronary artery no-reflow phenomena. Coronary artery no-reflow and inflammation related. Leukocytes, some inflammatory cytokines such as interleukin-6, interleukin-8, interleukin-10 and tumor necrosis factor-alpha, are involved in the process of coronary artery no-reflow and play an important role.