In vivo exposure of rat lungs to crystalline silica either by intratracheal instillation or by inhalation results in an increase in mRNA levels for inducible nitric oxide synthase (iNOS) in bronchoalveolar lavage cells (BALC), elevated nitric oxide (.NO) production by BALC, and an increase in.NO-dependent chemiluminescence (CL) from alveolar macrophages (AM).
Therefore, in vivo studies that involve short-term exposure of rat lungs to fibers and subsequent assessment of relevant endpoints, notably fibrosis, are probably adequately conservative for predicting long-term pathology – that is, will identify fibers that have a fibrogenic or carcinogenic potential (Bernstein et al., 2005c ).
The studies we report here represent part of our ongoing effort to characterize the immediate biologic responses of rat lung tissue to a toxic dose of O3 and to use this information to develop biomarkers for its toxicity (Hatch et al. 1986 , 1994.
In this study, we utilized a rat miRNA microarray containing 216 miRNA probes, printed in-house, to detect the expression of miRNAs in the rat lung compared to the rat heart, brain, liver, kidney and spleen.
Morphological studies of the rat lung exposed to 20 ppm NO2 for 20 hr (experiment 1), to 0.5 ppm for 19 months (experiment 2), and to 10 ppm for 14 days (experiment 3) were conducted.
In this study, we used a model of rat lung transplantation to test the hypothesis that chronic aspiration of gastric contents accelerates pulmonary allograft dysfunction.
In one study, apoptosis and parameters of infammation were measured after direct exposure of rat lung slices to DEE.
However, IL-13 and IL-β can act coordinately on rat lung myofibroblasts to enhance their proliferation.
Hypocapnia increases microvascular permeability and impairs alveolar fluid reabsorption in the isolated rat lung, due to an associated decrease in Na/K-ATPase activity [ 47].
