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Biomedical subjects

G Freeman

Publications and source records attributed to G Freeman.

At least 55 records · Page 3Linked to original sources
PubMed1978

Quantitation of damage to the alveolar epithelium by means of type 2 cell proliferation.

The purpose of this study was to determine whether the amount of alveolar epithelial tissue damaged during exposure of NO2 could be quantified by measuring the proliferative response to Type 2 cells. To accomplishe this, we used tissues from previously published experiments in which rats had been exposed to NO2 and the proliferative response to Type 2 cells had been measured during a 5-day period. The proportion of alveolar epithelium damaged was determined by stereologic examination with electron microscopy of tissue sections from those rats exposed to NO2 for 24 hours. These values were then compared with the total proliferative response to Type 2 cells for the 5 days of exposure. The study demonstrated that increasing tissue damage is assocaited with a greater proliferative response to Type 2 cells. The high degree of correlation (r = 0.93) indicates that the proliferative response of Type 2 cells can be used as an indirect means to quantify acute damage to the alveolar epithelium.

Animals↗
PubMed1978

Limited exposure of rats to H(2)SO(4) with and without O3.

The purpose of this study was to determine the effects of sulfuric acid (H(2)SO(4)) alone and with ozone (O(3)) on rats. To accomplish this, rats were exposed for 8 hours daily to an atmosphere containing either nebulized H(2)SO(4), H(2)SO(4) plus 0.9 ppm O(3), or 0.9 ppm O(3). The atmosphere in the exposure chambers was maintained at a fairly constant temperature and humidity. Nebulized H(2)SO(4) was delivered uniformly to provide a particle size of about 0.3 micron mass median diameter (MMD) and a mass concentration of 2 mg/m(3). In preliminary experiments, animals exposed to 2 mg/m(3) of H(2)SO(4) daily for 82 days showed very slight morphologic injury to the respiratory tract. In contrast, biological effects were readily demonstrable in rats exposed to H(2)SO(4) plus O(3) or to O(3) alone, possibly with some enhancement of effect in animals exposed to the mixture. The effects observed were characteristic of the response to O(3) alone.

Aerosols↗
PubMed1976

Renewal of the terminal bronchiolar epithelium in the rat following exposure to NO2 or O3.

Rats were exposed to either NO2 or O3 to determine whether nonciliated cells (Clara cells) could divide and differentiate into ciliated cells in the terminal bronchioles. Dividing cells were labeled with tritiated thymidine, visualized in the light and electron microscopes using autoradiographic techniques, and studied for up to 15 days after labeling. Electron microscopic autoradiography 1 hour after injection of tritiated thymidine showed that all labeled cells in the terminal bronchioles were nonciliated. However, 4 days after injection of tritiated thymidine, 67.8 per cent of the labeled cells were nonciliated and 32.2 per cent were ciliated. Light microscopic autoradiography showed that the new labeled ciliated cell population was stable for up to 15 days. These results indicate that nonciliated cells divide and the sister cells may form new ciliated and nonciliated cells. Thus, nonciliated cells can act as progenitor cells for the terminal bronchiolar epithelium.

Animals↗
PubMed1974

Early response of lung to low levels of ozone.

The epithelial response in the terminal bronchioles and alveoli was examined after exposure to approximately 0.5 and 0.9 ppm ozone (O(3)). Loss of ciliated cells from the terminal bronchiole was pronounced after 6 to 10 hours of exposure; however, nonciliated cells were resistant to injury from O(3). In contrast, type 1 alveolar lining cells were very sensitive to O(2) and were severely damaged or removed from significant areas of the proximal alveoli after as little as 2 hours of exposure to 0.5 ppm. The basement lamina was left devoid of an epithelium with the exception of type 2 cells, which were very resistant and retained a relatively normal appearance. Under continuous exposure, repair of the lesion area was accomplished in approximately 48 hours through proliferation of the type 2 cells. The new cells were cuboidal at first but subsequently became more squamous in appearance. Exposure for 8 to 10 hours followed by residence in clean air resulted in a proliferative response at 48 hours, about equal to that observed after continuous exposure.

Adaptation, Physiological↗