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60%氧气对弹性蛋白酶诱导的肺气肿仓鼠气腔扩大和交联弹性蛋白合成的影响。

The effect of 60% oxygen on air-space enlargement and cross-linked elastin synthesis in hamsters with elastase-induced emphysema.

作者信息

Cantor J O, Keller S, Cerreta J M, Manahan J, Evans H E, Turino G M

机构信息

Columbia University College of Physicians and Surgeons, New York, New York.

出版信息

Am Rev Respir Dis. 1990 Sep;142(3):668-73. doi: 10.1164/ajrccm/142.3.668.

DOI:10.1164/ajrccm/142.3.668
PMID:2117871
Abstract

Hyperoxia is routinely administered to patients with severe emphysema. To gain insight into the possibly adverse effects of such treatment, hamsters were exposed to 60% oxygen for 5 days, beginning 48 h after induction of pulmonary emphysema by intratracheal instillment of pancreatic elastase. Control groups consisted of (1) animals instilled with elastase and exposed to room air, (2) animals instilled with saline and exposed to 60% oxygen, and (3) animals instilled with saline and exposed to room air. Cross-linked elastin content and synthesis in the lung were measured immediately following termination of hyperoxia, and the mean linear intercept was determined 4 wk later. Cytologic examination of bronchoalveolar lavage fluids was also performed. Statistical significance was determined by a two-way analysis of variance. Results indicate that exposure to 60% oxygen significantly affected (p less than 0.05) air-space size, causing a 51% increase among elastase-treated hamsters (124 versus 82 microns) but only a 4% increment among saline-treated animals (52 versus 50 microns). When compared to other groups, animals treated with both elastase and hyperoxia had a significantly greater (p less than 0.01) percentage of neutrophils (28%) in their lung lavage fluids immediately following exposure to 60% oxygen. Although total lung elastin content was not altered by hyperoxia at this time, labelling of elastin cross-links was significantly increased (p less than 0.05). These studies demonstrate that exposure to 60% oxygen enhances elastase-induced lung injury. They also raise the possibility that oxygen therapy may, under certain circumstances, accelerate the progression of human emphysema.

摘要

重度肺气肿患者通常会接受高氧治疗。为深入了解这种治疗可能产生的不良反应,在通过气管内注入胰弹性蛋白酶诱导肺气肿48小时后,将仓鼠暴露于60%氧气环境中5天。对照组包括:(1)注入弹性蛋白酶并暴露于室内空气的动物;(2)注入生理盐水并暴露于60%氧气环境的动物;(3)注入生理盐水并暴露于室内空气的动物。在高氧暴露结束后立即测量肺中交联弹性蛋白的含量和合成情况,并在4周后测定平均线性截距。还对支气管肺泡灌洗液进行了细胞学检查。采用双向方差分析确定统计学意义。结果表明,暴露于60%氧气显著影响(p<0.05)气腔大小,弹性蛋白酶处理的仓鼠气腔大小增加了51%(从82微米增至124微米),而生理盐水处理的动物仅增加了4%(从50微米增至52微米)。与其他组相比,同时接受弹性蛋白酶和高氧处理的动物在暴露于60%氧气后,其肺灌洗液中的中性粒细胞百分比显著更高(p<0.01),为28%。虽然此时高氧并未改变肺弹性蛋白的总含量,但弹性蛋白交联的标记显著增加(p<0.05)。这些研究表明,暴露于60%氧气会加重弹性蛋白酶诱导的肺损伤。它们还提出了一种可能性,即在某些情况下,氧疗可能会加速人类肺气肿的进展。

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