Patterns of accumulation of platelets and neutrophils in rat lungs during exposure to 100% and 85% oxygen.
Patterns of accumulation of platelets and neutrophils in rat lungs during exposure to 100% and 85% oxygen.
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模式%20of%20累积%20of%20血小板%20和%20中性粒细胞%20在%20rat%20肺%20期间%20暴露%20至%20100%%20和%2085%%20氧气。
DOI：
10.1164/arrd.1985.132.3.548
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Crapo,JD
中科院分区：
文献类型：
--
作者：
Barry,BE;Crapo,JD
人们认为，高氧暴露期间白细胞流入肺部是导致肺泡损伤的一个重要因素，因为当它们被激活时，它们会通过产生氧自由基和释放水解酶来造成损伤。为了更好地了解高氧损伤与炎症反应之间的关系，采用形态测量方法定量暴露于100%和85%氧气的大鼠肺泡毛细血管血液成分的变化。在 100% 氧气中 40 小时后，毛细血管床中血小板的绝对体积增加了 78%，血小板覆盖的内皮细胞总表面积增加了 111%。在暴露于 100% O2 60 小时之前，中性粒细胞的这些参数没有显着变化。此时，中性粒细胞覆盖的绝对体积和内皮表面积都增加了三倍以上。在 85% 氧气中 3 天后，绝对血小板体积几乎增加了一倍，血小板覆盖的表面积增加了 79%。直到暴露于 85% 氧气 5 天后，中性粒细胞才出现增加，并且绝对体积和表面积在暴露 7 天后均降至低于对照值。在两次高氧暴露期间，中性粒细胞流入之前血小板的出现表明，最初的内皮细胞损伤是由于细胞内氧自由基产生增加造成的，而不是由于白细胞产生的氧自由基造成的。内皮细胞膜的变化与毛细血管床中血小板积聚的开始相关。血小板活化过程中释放的血小板成分可能是随后中性粒细胞流入的重要介质。中性粒细胞可能是氧中毒后期肺损伤的重要贡献者。与 100% 氧气中 60 小时相比，在 85% 氧气中 5 天后出现的中性粒细胞数量较少，可能是暴露于 85% 氧气的大鼠延长生存期的一个重要因素。
The influx of leukocytes into the lung during hyperoxic exposures has been suggested as a significant contributor to alveolar injury because, when activated, they can cause damage by producing oxygen radicals and releasing hydrolytic enzymes. To better understand the relationship between hyperoxic injury and inflammatory responses, morphometric methods were used to quantitate changes in alveolar capillary blood components of rats exposed to 100% and 85% oxygen. After 40 h in 100% oxygen the absolute volume of platelets in the capillary bed increased 78% and there was a 111% increase in the total endothelial cell surface area covered by platelets. There were no significant changes in these parameters for neutrophils until 60 h of exposure of 100% O2. At this point, both the absolute volume and the endothelial surface area covered by neutrophils increased more than threefold. After 3 days in 85% oxygen absolute platelet volume was almost doubled and the surface area covered by platelets increased 79%. No neutrophil increases occurred until 5 days exposure to 85% oxygen, and both absolute volume and surface area dropped to less than control values after 7 days of exposure. The appearance of platelets prior to an influx of neutrophils during both hyperoxic exposures suggests that the initial endothelial cell injury results from an increased intracellular production of oxygen radicals rather than being due to oxyen radicals produced by leukocytes. Endothelial cell membrane changes were associated with the initiation of platelet accumulation in the capillary bed. Platelet components released during platelet activation may be important mediators for the subsequent neutrophil influxes. Neutrophils are likely to be significant contributors to pulmonary injury in the later phases of oxygen toxicity. The smaller neutrophil population present after 5 days in 85% oxygen compared with 60 h in 100% oxygen may be an important factor for the prolonged survival of rats exposed to 85% oxygen.