Acute ozone-induced lung injury in rats: structural-functional relationships of developing alveolar edema.

Acute ozone-induced lung injury in rats: structural-functional relationships of developing alveolar edema.
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大鼠急性臭氧引起的肺损伤:肺泡水肿发展的结构功能关系。

DOI:
10.1016/0041-008x(92)90214-d
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发表时间:
1992
影响因子:
3.8
通讯作者:
Balis,JU
Balis,JU
中科院分区:
医学3区
文献类型:
--
作者:
Paterson,JF;Hammond,MD;Montgomery,MR;Sharp,JT;Farrier,SE;Balis,JU

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作为急性臭氧应激对肺表面活性物质系统影响的研究的一部分,我们将雄性大鼠暴露于3 ppm臭氧1、2、4和8小时后的肺损伤的形态测量、生化和功能指标相关联。结果显示,动态肺顺应性(ml/cmH 2 O/kg)显著降低,从对照值0.84 ± 0.02(SEM)分别降至4和8小时的0.72 ± 0.04和0.57 ± 0.06。在2小时时,PaO 2短暂升高至116 mmHg(对照= 92 mmHg),随后在4小时(65 mmHg)和8小时(55 mmHg)时降低。肺组织的形态测定,固定灌注固定剂通过肺动脉在12厘米水柱气道扩张压力,表现出增加的血管内室的面积在8小时,在与65和39%的肺泡面积的腹侧和背侧肺区域的液体分别取代。肺泡水肿与灌洗液中渗出蛋白呈正相关(r = 0.966)。以水肿为因变量的逐步多元回归模型表明,肺血管扩张、低氧血症和灌洗液中表面活性物质管状髓鞘的耗竭是预测肺泡水肿的指标。在第二个模型中,灌洗液蛋白浓度作为因变量,降低动态顺应性和低氧血症是进行性肺泡内血浆蛋白渗出的预测因子。上述结构-功能关系支持臭氧诱导的高蛋白肺泡水肿与肺充血、表面活性剂小管髓鞘缺乏和相关肺功能障碍在病理上相关的概念。
As part of a study on the effects of acute ozone stress on the lung surfactant system, we correlated morphometric, biochemical, and functional indices of lung injury using male rats exposed to 3 ppm ozone for 1, 2, 4, and 8 hr. Evaluation of lung mechanics, using the Pulmonary Evaluation and Diagnostic Laboratory System, revealed a significant decrease in dynamic lung compliance (ml/cmH2O/kg) from a control value of 0.84 ± 0.02 (SEM) to 0.72 ± 0.04 and 0.57 ± 0.06 at 4 and 8 hr, respectively. At 2 hr there was a transient increase in PaO2to 116 torr (control = 92 torr) followed by a decrease at 4 hr (65 torr) and 8 hr (55 torr). Morphometry of lung tissue, fixed by perfusion of fixative via the pulmonary artery at 12 cm H2O airway distending pressure, demonstrated an increase in the area of the intravascular compartment at 8 hr, in association with a 65 and 39% replacement of the alveolar area by fluid in ventral and dorsal lung regions, respectively. There was a positive correlation (r = 0.966) between alveolar edema and transudated proteins in lavage fluid. A stepwise multiple regression model, with edema as the dependent variable, suggested that pulmonary vasodilatation, hypoxemia, and depletion of surfactant tubular myelin in lavage fluid were indices for predicting alveolar edema. In a second model, with lavage protein concentration as the dependent variable, decreasing dynamic compliance and hypoxemia were predictors of progressive, intraalveolar transudation of plasma proteins. The above structural-functional relationships support the concept that ozone-induced high-protein alveolar edema is pathogenetically linked to pulmonary hyperemia, deficiency of surfactant tubular myelin, and associated lung dysfunctions.
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