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Biomedical subjects

W S Tyler

Publications and source records attributed to W S Tyler.

At least 55 records · Page 3Linked to original sources

Short term morphologic effects of high ambient levels of ozone on lungs of rhesus monkeys.

Groups of laboratory-reared, young adult rhesus monkeys were exposed to 0.8 p.p.m. or 0.5 p.p.m. of ozone for 8 hours a day on 7 consecutive days. Lesions were studied using correlated techniques which permitted examination of specified levels of airways and adjacent lung parenchyma by light microscopy, scanning electron microscopy, and transmission electron microscopy. Lesions were observed in the trachea and lungs of all exposed animals. The extent and severity of damage, but not its nature, varied with exposure concentration. Damage was most severe in respiratory bronchioles and more distal parenchymal regions were unaffected. Major features of the response within respiratory bronchioles were hyperplasia and hypertrophy of nonciliated bronchiolar epithelial cells and intraluminal accumulations of macrophages. Replacement of type 1 epithelium in alveoli by type 2 cells and forms intermediate between types 1 and 2 were also observed. In large conducting airways, damage to ciliated cells was observed but mlcus-producing cells were morphologically unaltered. Two gradients in severity of ozone-induced lesions were appreciable in the trachea and lungs. The most obvious gradient was in respiratory bronchioles where the degree of damage was most severe in proximal locations. A second gradient in severity was noted in conducting airways in which more severe and extensive lesions occurred in the trachea and major bronchi than in small bronchi and terminal bronchioles.

Air Pollutants↗

Effect of a congenital defect in hemopoiesis on myeloid growth and the stem cell (CFU) in an in vivo culture system.

W/Wv mice with congenitally defective CFU proliferation and their normal, congenic littermates were used as hosts for diffusion chamber (DC) implants. CFU growth in implanted allogenic CF1, or congenic +/+ marrow was significantly greater in W/Wv than in control hosts. When W/Wv mice were "cured" of their hemopoietic defect, CFU proliferation in the DCs decreased, but not to the control level. These observations have provided evidence for humoral control of CFU growth related to a genetic stem cell defect. Diffusion chamber myelopoiesis was also enhanced in W/Wv hosts. In comparison with their congenic controls, W/Wv mice were neutropenic and had decreased numbers of marrow myeloid elements. Thus, a humorally mediated feedback related to a defective myelopoiesis in the hosts might have accounted for increased DC myelopoiesis. However, a "spillover" effect from increased stem cell growth has not been excluded.

Anemia, Macrocytic↗

Pulmonary responses of rats to ambient levels of ozone: effects of 7-day intermittent or continuous exposure.

Groups of Sprague-Dawley rats were exposed to ozone for either 8 or 24 hours a day for 7 consecutive days to evaluate morphologic changes of the respiratory system. Three levels of exposure (0.2, 0.5, and 0.8 p.p.m. of O3) were selected to simulate moderate to severe episodes of oxidant pollution in urban environments. Morphologic evaluation included light, scanning electron, and transmission electron microscopy. Biochemical parameters which were examined included succinate oxidase, glucose-6-phosphate dehydrogenase, and nicotinamide adenine dinucleotide phosphate-cytochrome c reductase activities. The results indicated that (1) exposure to concentrations as low as 0.2 p.p.m. for 7 days induced pulmonary damage; (2) there was a dose-dependent pulmonary response to the three levels of ozone which was quantitated by alterations in biochemical marker enzyme activities and observed morphologically; (3) proportionate differences were not observed in morphologic characteristics of the lesions or detected in biochemical parameters between rats exposed continuously for 7 days and those exposed intermittently for 8 hours a day for 7 consecutive days; (4) alterations in surface height and granularity of the cytoplasmic luminal projection of Clara cells were subtle changes which were dose-dependent, occurring even at the lowest ozone concentration, and best detected by scanning electron microscopy; (5) alveolar macrophage accumulation within proximal alveoli of alveolar ducts was the most readily detectable morphologic indicator of pulmonary damage; and (6) although the brunt of ozone damage was borne by the centriacinar region, there was damage to cilia and increased ciliogenesis occurring in the trachea and larger conducting airways following exposure of 0.5 and 0.8 p.p.m. of ozone.

Air Sacs↗

Intrapulmonary airway morphology in three species of monkeys: a correlated scanning and transmission electron microscopic study.

Intrapulmonary airways were studied in rhesus (Macaca mulatta), stumptail (Macaca arctoides), and bonnet (Macaca radiata) monkeys by correlated scanning and transmission electron microscopy. Lobar, segmental, and subsegmental bronchi in all three macaques were lined by pseudostratified columnar epithelium composed primarily of ciliated cells, mucous cells, and basal cells. Neuronal processes and cells containing dense-core vesicles were also observed. Terminal bronchioles in bonnet and stumptail monkeys were lined by ciliated pseudostratified columnar epithelium which included nonciliated branchiolar epithelial (Clara) cells. The arrangement of epithelium in terminal bronchioles differed slightly in rhesus monkeys. All three species had long respiratory bronchioles. They were lined by simple, nonciliated cuboidal and squamous epithelium which usually did not contain secretory droplets. Capillaries were often observed immediately below the luminal epithelium. Cuboidal cells containing dense-core vesicles were a rare component of the epithelium of respiratory bronchioles in stumptail monkeys. Alveolar ducts were lined by an epithelium composed of type I and type II cells. The results of this study indicate that there is general similarity in the mucosal structure of bronchi and respiratory bronchioles between macaques and man but that there are differences in the number of generations and epithelial lining of terminal bronchioles.

Animals↗

Pulmonary lesions in rats exposed to ozone. A correlated light and electron microscopic study.

Selective embedding processes were used to identify lesions in different regions of pulmonary acini in a histologic and ultrastructural study of the effects of a 4-hour exposure to 3 ppm ozone on rat lungs. There was a gradation of epithelial damage in acini; the severest lesions were located centrally, where there was necrosis of bronchiolar epithelium and membranous pneumonocytes. In peripheral acinar regions, membranous cells were normal; granular pneumonocytes were normal throughout. In contrast, lesions in capillary endothelium were more wide-spread. Endothelial swelling was seen in all portions of acini, but was more common centrally, and ring-like formations of endothelial membranes were found peripherally. Early stages of alveolar edema were more often seen in peripheral acinar regions and were usually accompanied by interstitial edema. These results confirm that the brunt of ozone damage is borne by centriacinar regions. Further, they highlight the need to identify portions of acini being examined ultrastructurally to avoid variable and conflicting results. The apparent separation of centriacinar epithelial damage from the peripheral location of the earliest detectable edema indicates that further exploration is needed to determine to what extent different, although overlapping, sets of pathogenetic factors might be involved.

Animals↗

Morphometric evaluation of pulmonary lesions in rats exposed to ozone.

Four hours exposure to 3 ppm ozone produces morphometrically quantifiable alterations in the lungs of rats. Lungs of exposed rats were fixed either immediately after exposure or after a 12-hour recovery period, and the tissue was evaluated using stereologic technics with both the light and electron microscopes. Immediately after exposure, the volume fraction of nonparenchymal tissue was larger (0.057) than for controls (0.045); that of the lumina of large vessels decreased (0.039) from the control value (0.059). The nonparenchymal tissue fraction was 0.053 12 hours later, while the luminal fraction (0.054) resembled the control value. The volume fractions of parenchyma, total tissue and air space showed only slight changes. Ozone also affects all three components of the air-blood barrier, primarily by the production of intracellular edema. The arithmetic mean thickness of the pulmonary blood-air barrier increased from 1.385 +/- 0.095 mu in unexposed rats to 1.700 +/- 0.189 mu in rats immediately after exposure. The primary increase was in thickness of membranous epithelial and capillary endothelial cells. Partial recovery of total barrier thickness (1.582 +/- 0.292 mu) occurred 12 hours after exposure.

Animals↗