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吸入一氧化氮可防止过氧化氢引起的肺血管通透性增加。

Inhaled nitric oxide prevents the increase in pulmonary vascular permeability caused by hydrogen peroxide.

作者信息

Poss W B, Timmons O D, Farrukh I S, Hoidal J R, Michael J R

机构信息

Department of Medicine, Veterans Affairs Medical Center, Salt Lake City, Utah, USA.

出版信息

J Appl Physiol (1985). 1995 Sep;79(3):886-91. doi: 10.1152/jappl.1995.79.3.886.

DOI:10.1152/jappl.1995.79.3.886
PMID:8567532
Abstract

Given the interest in using inhaled nitric oxide (NO.) to treat acute lung injury and the importance of oxygen radicals in its pathogenesis, we studied the effects, in buffer-perfused isolated rabbit lungs, of inhaled NO. (24 ppm) on the injury caused by generating hydrogen peroxide with glucose and glucose oxidase (GOX). Experiments were performed at a constant pulmonary arterial pressure. GOX substantially augmented vascular permeability, as demonstrated by an increase in the lung-to-perfusate 125I-labeled albumin ratio, lavage-to-perfusate 125I-albumin ratio, wet-to-dry lung weight ratio, and pulmonary vascular filtration coefficient. Lungs treated with inhaled NO. before perfusion with GOX had lung-to-perfusate and lavage-to-perfusate 125I-albumin ratios that were not significantly different from control values and intermediate between the control and GOX groups. Inhaled NO. also prevented the increase in wet-to-dry lung weight ratio and pulmonary vascular filtration coefficient caused by GOX.. Thus inhaled NO. substantially reduced in the isolated lung the increase in pulmonary vascular permeability produced by the intravascular generation of hydrogen peroxide.

摘要

鉴于使用吸入一氧化氮(NO.)治疗急性肺损伤的研究兴趣以及氧自由基在其发病机制中的重要性,我们在缓冲液灌注的离体兔肺中研究了吸入NO.(24 ppm)对葡萄糖和葡萄糖氧化酶(GOX)产生过氧化氢所引起损伤的影响。实验在恒定肺动脉压下进行。GOX显著增加了血管通透性,表现为肺与灌注液中125I标记白蛋白比率、灌洗与灌注液中125I白蛋白比率、肺湿重与干重比率以及肺血管滤过系数增加。在灌注GOX之前用吸入NO.处理的肺,其肺与灌注液以及灌洗与灌注液中125I白蛋白比率与对照值无显著差异,且介于对照组和GOX组之间。吸入NO.还可防止GOX引起的肺湿重与干重比率以及肺血管滤过系数增加。因此,吸入NO.可显著减轻离体肺中血管内产生过氧化氢所导致的肺血管通透性增加。

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