Changes in lung and systemic oxidant and antioxidant activity after smoke inhalation.
Changes in lung and systemic oxidant and antioxidant activity after smoke inhalation.
复制标题
吸入烟雾后肺部和全身氧化剂和抗氧化活性的变化。
DOI：
10.1097/00024382-199402000-00004
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Blanchard,J
中科院分区：
文献类型：
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作者：
Demling,R;Lalonde,C;Picard,L;Blanchard,J
我们测定了肺气道、实质和全身组织对烟雾吸入的反应的氧化活性，并将脂质过氧化与生理和组织学变化进行比较。成年羊被给予控制量的来自燃烧的棉毛巾的冷却烟雾，其中含有3-4μm的均匀颗粒直径。平均峰值碳氧血红蛋白为 45+/-4%。动物在未麻醉的情况下监测24小时并处死。由于气道粘膜溃疡、粘膜下水肿和肺不张，以及气道液体增加，但肺泡水肿轻微，出现严重呼吸衰竭。气道液丙二醛（MDA）含量是血浆的三倍。然而，气道粘膜和肺实质组织、脂质过氧化和氧化型谷胱甘肽并未增加，表明唯一的直接氧化剂活性仅存在于气道表面。除氧化剂外，其他因素也可能与肺损伤有关。然而，肝组织 MDA 显着增加以及还原型谷胱甘肽和过氧化氢酶活性降低证明了显着的全身氧化应激。组织氧化应激还导致全身耗氧量增加 75%，软组织血管通透性增加。我们的结论是：1）在气道液体中注意到吸烟后唯一的直接肺氧化应激，而尽管存在严重气道损伤和肺不张，但并未观察到肺组织脂质过氧化，2）除了全身组织氧化应激的证据外，烟雾暴露还观察到主要的全身生理变化，如全身需氧量增加和全身微血管通透性增加所证明的。氧化剂活性的可能来源是烟雾引起的全身炎症。
We determined the oxidant activity in lung airways, parenchyma, and systemic tissues in response to smoke inhalation, comparing lipid peroxidation with physiologic and histologic change. Adult sheep were given a controlled amount of cooled smoke from burned cotton toweling, containing a uniform particle diameter of 3-4 [mu] m. The mean peak carboxyhemoglobin was 45+/-4%. Animals were monitored unanes-thetized for 24 h and killed. Severe respiratory failure was noted, as a result of airways mucosal ulceration, submucosal edema, and atelectasis, along with increased airways fluid, but minimal alveolar edema. Airway fluid malondialdehyde (MDA) content was threefold greater than plasma. However, airways mucosa and lung parenchymal tissue, lipid peroxidation, and oxidized glutathione were not increased, suggesting the only direct oxidant activity was present only at the airways surface. Other factors besides oxidants are likely to be involved in the lung injury. However, a marked systemic oxidant stress was noted as evidenced by a significant increase in liver tissue MDA and decrease in reduced glutathione and catalase activity. The tissue oxidant stress also corresponded with a 75% increase in systemic oxygen consumption and an increase in soft tissue vascular permeability. We conclude that: 1) the only direct lung oxidant stress after smoke was noted in airways fluid, while lung tissue lipid peroxidation was not seen despite severe airways injury and atelectasis, and 2) major systemic physiologic changes, as evidenced by increased systemic oxygen demands and systemic micro-vascular permeability are seen with smoke exposure in addition to evidence of systemic tissue oxidant stress. The likely source of the oxidant activity was a smoke-induced systemic inflammation.