Free radical and granulocyte-mediated injury during myocardial ischemia and reperfusion.
Free radical and granulocyte-mediated injury during myocardial ischemia and reperfusion.
复制标题
心肌缺血和再灌注期间自由基和粒细胞介导的损伤。
DOI：
10.1016/0002-9149(89)90225-7
复制
发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Engler,RL
中科院分区：
文献类型：
--
作者：
Engler,RL
溶栓/再灌注治疗在限制心肌梗死范围方面的成功可能受到再灌注损伤的限制。急性缺血的损伤不仅仅是由于血流中断;相反，缺血引发了一系列反应，包括部分减少的氧气、炎症介质、粒细胞造成的机械性毛细血管阻塞和其他导致不可逆损伤的事件。一个令人惊讶的结果是，通过输送氧气和粒细胞进行再灌注可能会抵消恢复血流的一些好处。中性粒细胞和自由基损伤的机制包括超氧化物自由基形成和脂质过氧化、进行性白细胞毛细血管堵塞和毛细血管无复流以及水肿。心脏中各种特定损伤机制的相互作用（即，黄嘌呤氧化酶、线粒体超氧化物泄漏、嗜中性粒细胞超氧化物、脱粒和毛细血管堵塞以及嗜中性粒细胞衍生的血管收缩剂）值得进一步研究。
The success of thrombolytic/reperfusion therapy in limiting the extent of myocardial infarction may be limited by reperfusion injury. Damage from acute ischemia is not due solely to the interruption of blood flow; rather, ischemia initiates a cascade of reactions involving partially reduced oxygen, inflammatory mediators, mechanical capillary obstruction by granulocytes and other events that lead to irreversible injury. A surprising consequence is that reperfusion by delivering oxygen and granulocytes may counteract some of the benefits of restoring flow. Mechanisms of neutrophil and free radical injury include superoxide radical formation and lipid peroxidation, progressive leukocyte capillary plugging and capillary no-reflow, and edema. The interaction of various specific mechanisms of injury in the heart (i.e., xanthine oxidase, mitochondrial superoxide leak, neutrophil superoxide, degranulation and capillary plugging, and neutrophil-derived vasoconstrictors) deserves further study.