Department of Anesthesiology, Stomatology Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, China.
J Surg Res. 2010 Nov;164(1):131-8. doi: 10.1016/j.jss.2008.09.017. Epub 2008 Oct 14.
The aim of this study was to investigate the post-treatment effect of intravenous hyperoxygenated solution (HOS) on pulmonary parameters in rabbits whole-body-exposed to the toxic gas phosgene.
Twenty-four New Zealand rabbits were divided into four groups randomly: rabbits were exposed whole-body to either filtered room air or 539 ppm phosgene for 5 minutes followed by room air washout for 5 minutes. Phosgene-exposed group (exposed to phosgene without treatment, PH group); Control group (exposed to air, Control group); Lactate Ringer's solution (LRS)-treated group (intravenous infusion of LRS by 30 ml·kg-1 after phosgene exposure, LRS group); Hyperoxygenated solution (HOS)-treated group (intravenous infusion of HOS after phosgene exposure by 30 mL·kg-1, HOS group). Arterial blood was collected for blood gas analysis at 1, 3, 8, and 12 hours after phosgene or air exposure. Rabbits were put to death 12 hours after exposure. Lung edema was assessed gravimetrically by measuring tissue wet/dry weight ratio (W/D) and lung coefficient (LC). Bronchoalveolar lavage (BAL) was performed and fluid was analyzed for total maloaldehyde (MDA), glutathione peroxidase (GSH-Px), and protein concentration. Lungs were perfused with saline to remove blood, snap-frozen in liquid nitrogen (N2), analyzed for tissue reduced glutathione (GSH) and oxidized glutathione (GSSG). Parts of lung tissues were reserved for histopathology examination.
In the PH, LRS, and HOS groups, phosgene inhalation caused serious lung edema, W/D and LC, lung tissue GSSG, BALF MDA, and protein content increased significantly. Meanwhile, PaO2, lung tissue GSH, and BALF GSH-Px decreased markedly. However, after HOS treatment in the HOS group, PaO2 was clearly higher than that in the PH group and LRS group at 3, 8, 12 hours (P < 0.01). W/D and LC, lung tissue GSSG, BALF MDA, and protein content in the HOS group were apparently lower than that in the PH group and LRS group (P < 0.01). In the HOS group, lung tissue GSH and BALF GSH-Px increased compared with both PH and LRS group, respectively. There was no difference on lung tissue GSH among the PH, LRS, and HOS groups (P > 0.05).
Intravenous HOS infusion after phosgene exposure can clearly lessen phosgene-induced lung edema formation, lipid peroxidatic reaction, and ameliorate hypoxemia associated with phosgenismus; it is a safe, simple, and effective measure to protect animals from phosgene-induced lung injury.
本研究旨在探讨全身暴露于光气后的静脉高氧溶液（HOS）对兔肺参数的治疗后效果。
将 24 只新西兰兔随机分为四组：兔全身暴露于过滤空气或 539ppm 光气中 5 分钟，然后用空气冲洗 5 分钟。光气暴露组（暴露于光气而未治疗，PH 组）；对照组（暴露于空气，对照组）；乳酸林格氏液（LRS）治疗组（光气暴露后静脉输注 30ml·kg-1 的 LRS，LRS 组）；高氧溶液（HOS）治疗组（光气暴露后静脉输注 30ml·kg-1 的 HOS，HOS 组）。在光气或空气暴露后 1、3、8 和 12 小时采集动脉血进行血气分析。暴露后 12 小时处死兔子。通过测量组织湿/干重比（W/D）和肺系数（LC）来评估肺水肿的重量。进行支气管肺泡灌洗（BAL），并分析总丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH-Px）和蛋白浓度。用生理盐水冲洗肺以清除血液，将肺组织迅速冷冻在液氮（N2）中，分析组织还原型谷胱甘肽（GSH）和氧化型谷胱甘肽（GSSG）。保留部分肺组织进行组织病理学检查。
在 PH、LRS 和 HOS 组中，光气吸入导致严重的肺水肿，W/D 和 LC、肺组织 GSSG、BALF MDA 和蛋白含量显著增加。同时，PaO2、肺组织 GSH 和 BALF GSH-Px 明显下降。然而，在 HOS 组中，与 PH 组和 LRS 组相比，HOS 组在 3、8、12 小时时 PaO2 明显升高（P<0.01）。W/D 和 LC、肺组织 GSSG、BALF MDA 和蛋白含量明显低于 PH 组和 LRS 组（P<0.01）。在 HOS 组中，肺组织 GSH 和 BALF GSH-Px 分别高于 PH 组和 LRS 组。PH、LRS 和 HOS 组之间肺组织 GSH 无差异（P>0.05）。
光气暴露后静脉输注 HOS 可明显减轻光气引起的肺水肿形成、脂质过氧化反应，并改善光气中毒相关的低氧血症；这是一种安全、简单、有效的措施，可保护动物免受光气引起的肺损伤。
