目的观察几种长效局麻药对多形核中性粒细胞(PMN)释放氧自由基的抑制作用。
Objective to study the inhibitory effects of some local anesthetics on oxygen free radicals generation of polymorphonuclear neutrophils (PMNs) and its possible mechanisms.
目的：观察流感病毒对小鼠肺灌流液中免疫细胞释放氧自由基水平的影响及药物调节作用。
Objective:To study on effect of influenza virus on reactive oxygen species level release from immunocytes in perfusion liquid from mouse's lung and regulation of drugs.
这种情况发生的原因是身体机能接触氧后产生的副产物自由基的释放，自由基是一类具有高活性的分子，对人体具有巨大的威胁。
This happens because of exposure to free radicals, highly reactive molecules that are byproducts of bodily functions involving oxygen (which is just about all of them).
快速老化是由氧自由基的释放引起的。
This rapid aging process is caused by the release of free oxygen radicals.
其中中性粒细胞在肺内蓦集，释放蛋白酶、氧自由基等毒性物质是一重要发病机制。
Among various inflammatory mediators neutrophil is thought to be a major pathogenesis by accumulation in distal airway and secreting elastase and oxygen-free radicals.
作为宿主抵抗感染的主要防御细胞，中性粒细胞具有趋化、吞噬、产生氧自由基及释放作用等生物学特性。
As the main defense cell of the host immune response, neutrophils present lots of biological behaviors such as chemotaxis, phagocytosis, generating oxygen free radicals and so on.
心肌缺血再灌注损伤的主要机制为氧自由基大量释放，细胞内钙超载以及缺血导致的大量儿茶酚胺释放。
The mechanism of myocardium ischemia reperfusion injury involve in generating of reactive oxygen species, overload of Ca2 + and releasing of catecholamine by ischemia.
心肌缺血再灌注损伤的主要机制为氧自由基大量释放，细胞内钙超载以及缺血导致的大量儿茶酚胺释放。
The mechanism of myocardium ischemia reperfusion injury involve in generating of reactive oxygen species, overload of Ca2 + and releasing of catecholamine by ischemia.
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