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暴露于有毒氧水平的大鼠肺结缔组织的损伤与修复

Damage and repair of lung connective tissue in rats exposed to toxic levels of oxygen.

作者信息

Riley D J, Kramer M J, Kerr J S, Chae C U, Yu S Y, Berg R A

出版信息

Am Rev Respir Dis. 1987 Feb;135(2):441-7. doi: 10.1164/arrd.1987.135.2.441.

Abstract

We studied damage and repair of lung connective tissue in rats exposed to toxic amounts of oxygen by measuring lung content of collagen and elastin and the number of collagen fragments in lung lavage fluid after exposure to 98% O2 for 60 h. Lung collagen was decreased 17%, and collagen fragments in lavage fluid were increased 4- to 5-fold in O2-exposed rats compared with those in control rats. No biochemical evidence of elastin degradation was found. Mild emphysematous changes and a leftward shift of fluid-filled, pressure-volume curves were induced within 2 wk after recovery from exposure to O2. Administration of the lathyrogen beta-aminopropionitrile worsened the emphysematous lesion produced by hyperoxia, suggesting that replacement of connective tissue during repair limits the extent of emphysema. We conclude that lung collagen is degraded and an emphysematous lesion is produced by relatively short exposure to toxic amounts of oxygen.

摘要

我们通过测量暴露于有毒剂量氧气的大鼠肺组织中胶原蛋白和弹性蛋白的含量以及肺灌洗液中胶原片段的数量,研究了大鼠肺结缔组织的损伤和修复情况。将大鼠暴露于98%氧气中60小时后,与对照大鼠相比,暴露于氧气的大鼠肺胶原蛋白含量降低了17%,灌洗液中的胶原片段增加了4至5倍。未发现弹性蛋白降解的生化证据。从氧气暴露中恢复后2周内,出现了轻度肺气肿变化以及充满液体的压力-容积曲线向左移位。给予致畸形物β-氨基丙腈会使高氧引起的肺气肿病变恶化,这表明修复过程中结缔组织的替代限制了肺气肿的程度。我们得出结论,相对较短时间暴露于有毒剂量的氧气会导致肺胶原蛋白降解并产生肺气肿病变。

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