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二氧化氮诱导的大鼠肺气肿。β-氨基丙腈治疗未导致病情恶化。

Nitrogen-dioxide-induced emphysema in rats. Lack of worsening by beta-aminopropionitrile treatment.

作者信息

Blank J, Glasgow J E, Pietra G G, Burdette L, Weinbaum G

机构信息

Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia.

出版信息

Am Rev Respir Dis. 1988 Feb;137(2):376-9. doi: 10.1164/ajrccm/137.2.376.

Abstract

We evaluated the effect of beta-aminopropionitrile (beta APN) on the nitrogen dioxide (NO2) animal model of emphysema. Rats maintained on a beta APN-supplemented or a regular diet were exposed to 30 ppm NO2 for intervals ranging from 1 to 8 wk. Emphysema development was assessed by histologic evaluation and by changes in lung volume and mean linear intercept values. Evidence of pathologic changes were also documented by clinical and radiographic findings of osteolathyrism. The induction of centriacinar emphysema was attributed specifically to NO2 exposure. Neither the severity of the emphysema nor the time course of its development was altered by the beta APN-supplemented diet. These findings are in marked contrast to those observed with the exogenous elastase model of the disease, and they suggest that elastin synthesis and repair may not modulate elastin destruction in the NO2 model of emphysema.

摘要

我们评估了β-氨基丙腈(β-APN)对二氧化氮(NO2)诱导的肺气肿动物模型的影响。将食用补充β-APN或常规饮食的大鼠暴露于30 ppm的NO2中,暴露时间为1至8周。通过组织学评估以及肺体积和平均线性截距值的变化来评估肺气肿的发展。骨生成异常的临床和影像学表现也记录了病理变化的证据。中央型肺气肿的诱导具体归因于NO2暴露。补充β-APN的饮食既未改变肺气肿的严重程度,也未改变其发展的时间进程。这些发现与该疾病的外源性弹性蛋白酶模型所观察到的结果形成鲜明对比,并且表明在肺气肿的NO2模型中,弹性蛋白的合成和修复可能不会调节弹性蛋白的破坏。

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