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
中科院分区:
文献类型:
--
作者:
Paterson,JF;Hammond,MD;Montgomery,MR;Sharp,JT;Farrier,SE;Balis,JU
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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影响因子:
4
作者:
M. Sliwkowski;J. Lofgren;G. Lewis;T. Hotaling;B. Fendly;J. Fox
通讯作者:
M. Sliwkowski;J. Lofgren;G. Lewis;T. Hotaling;B. Fendly;J. Fox
影响因子:
11.2
作者:
A. Eisenthal;Robert B. Cameron;I. Uppenkamp;S. A. Rosenberg
通讯作者:
S. A. Rosenberg
影响因子:
4.4
作者:
M. Potapnev;T. S. Garbuzenco;N. Goncharova;V. D. Zobnin;O. V. Shadrin;S. Bykovskaya
通讯作者:
S. Bykovskaya
影响因子:
2
作者:
K. Ohta;Y. Yamaguchi;K. Shimizu;E. Miyahara;T. Toge
通讯作者:
T. Toge
影响因子:
56.9
作者:
SLAMON, DJ;GODOLPHIN, W;PRESS, MF
通讯作者:
PRESS, MF