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Biomedical subjects

W S Tyler

Publications and source records attributed to W S Tyler.

At least 37 records · Page 2Linked to original sources
PubMed1987

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. I. Clinical profile of horses.

Detailed physical and clinical examinations were performed on 26 Thoroughbred racehorses which were used subsequently in a series of studies to investigate the contribution of the pulmonary and bronchial arterial circulations to the pathophysiology of exercise-induced pulmonary haemorrhage (EIPH). Twenty-five of the horses had been retired from race training in Hong Kong during the 1984-85 season, all but four raced that season; one horse had been retired the previous season. The average number of races for the group that season was 4.1 +/- 2 with an average distance of 1502 +/- 216 metres, mean racing speed 15.5 +/- 0.5 metres/sec. Time from last race to necropsy was 177 +/- 155 days, range 12 to 572 days. All but one horse had a known history of either EIPH or epistaxis. Time from last recorded incident of expistaxis (17 horses) to necropsy was 156 +/- 141 days, range 12 to 513 days, with a longer interval since last recorded endoscopic observation of EIPH. Focal abnormal lung sounds were detected in the dorsocaudal lungfields on auscultation during rebreathing in three horses and six had tracheobronchial cytology consistent with previous episodes of pulmonary haemorrhage (haemosiderophages). No other characteristics which might have allowed separation of this group of horses from other Thoroughbred horses recently in race training were identified.

Animals↗
PubMed1987

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. II. Gross lung pathology.

Gross post mortem examinations were performed on the lungs of 26 Thoroughbred horses of known exercise-induced pulmonary haemorrhage (EIPH) status. The most consistent finding was a variable degree of bilaterally symmetrical, dark discolouration of the dorsocaudal regions of the caudal lung lobes. In more severely affected lungs, the stained areas extended cranially along the dorsal surfaces of the lungs, and in some cases affected approximately one third of the lung surface. Discoloured areas of lung were denser than normal, collapsed less readily, often contained trapped air and were slow to inflate. The subpleural bronchial arteries were more prominent in the discoloured regions. Pleural adhesions were noted in two horses but were not related to the discoloured lung regions. It was concluded that the discoloured lesions have a complex pathogenesis and were related directly to previous bouts of EIPH. Associated with them were signs indicating probable partial small airway obstruction, decreased tissue compliance and direct involvement of the bronchial arterial circulation.

Animals↗
PubMed1987

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. III. Subgross findings in lungs subjected to latex perfusions of the bronchial and pulmonary arteries.

Latex was injected under pressure into bronchial and pulmonary arteries of the inflated lungs of Thoroughbreds and transverse sections taken to calculate the area of lesions resulting from exercise-induced pulmonary haemorrhage. Extensive areas of dense brown haemosiderin varying from 0 to 45 per cent of total lung volume were identified, predominantly in the dorsocaudal lungfields. Bronchial arterial proliferation appeared to have replaced the pulmonary supply in affected areas of the lung. Closely associated with the staining and bronchial arterialisation, there was widespread small airway disease. The most severely affected bronchioles contained thick gelatinous or mucous exudate or mucoid plugs and had grossly thickened walls. These lesions suggest that the source of haemorrhage in exercise-induced pulmonary haemorrhage is from alveolar capillaries anomalously supplied by the bronchial arterial circulation through the development of pathological shunts. Small airway disease is suggested as being of major importance in the pathogenesis of the disease and may have led to the initial proliferation of the bronchial circulation.

Animals↗
PubMed1987

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. IV. Changes in the bronchial circulation demonstrated by C.T. scanning and microradiography.

The purpose of this study was to use radiographic contrast techniques and special imaging methods to identify and high-light bronchial arterial involvement in lung lesions associated with exercise-induced pulmonary haemorrhage (EIPH) in horses. The lungs from four horses with histories of EIPH were prepared for computerised tomographic scanning and microradiography by perfusing the broncho-oesophageal artery with a mixture of red latex and either barium or iodine contrast materials while the pulmonary supply received only blue latex. Computerised tomographic scan slices of the prepared inflated lungs were obtained from the caudal tip of the lung to the hilus. Microradiography of selected lung slices was also performed on a Faxitron. Diffuse areas of increased density, with preferential bronchial arterial supply noted on the computerised tomographic scans were confirmed by microradiography. Dense focal and diffuse plexuses of markedly hypertrophied and highly branched bronchial arterial networks were identified, centred around certain small airways. The vascular supply to these plexuses was recruited predominantly from neighbouring bronchial vessels, and in some cases, from the enlarged vasa vasorum of pulmonary arteries sending anastomoses to the affected areas. The authors conclude that bronchial vascular lesions in EIPH cases are the likely origin of haemorrhage; that small airway disease is the probable initiating stimulus for bronchial vascular proliferation in these lesions; and that the morphology and nature of the neovascular tissue in these lesions provides the conditions leading to haemorrhage in the lungs of horses with EIPH.

Animals↗
PubMed1987

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. V. Microscopic observations.

Lungs from 19 Thoroughbred racehorses with a history of exercise-induced pulmonary haemorrhage (EIPH) were studied using several forms of microscopy. Light microscopy of paraffin sections revealed three lesions in the caudodorsal region of the lungs from each horse. These correspond with the location of blue to brown stains seen at necropsy. These lesions include sequelae of bronchiolitis, hemosiderophages and increased connective tissue. Much of each of the lungs appeared normal, especially the more cranial or ventral portions. Foci of eosinophil infiltration were found in seven of the 19 lungs examined. With two exceptions, these eosinophilic foci had a different distribution to the three lesions. In areas of severe bronchiolar changes and fibrosis, vascular lesions typical of hypertension were found occasionally. Transmission electron microscopy was used to confirm cell types seen by light microscopy and to examine arterioles for changes characteristic of neovascularisation. Areas of enlarged airspaces from the vascular injected right lungs were examined by scanning electron microscopy. The balance of fibrosis and destruction varied in these areas, but none were as extensive as those seen in chronic obstructive pulmonary disease. The authors hypothesise that bronchiolitis and related neovascularisation are essential components of the aetiology of EIPH.

Animals↗
PubMed1987

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VIII. Conclusions and implications.

This paper reviews a series of clinical, post mortem and imaging studies on exercise-induced pulmonary haemorrhage (EIPH) performed on 26 Thoroughbred racehorses. Post mortem techniques included routine gross, subgross and histological examination; coloured latex perfusions of pulmonary and bronchial circulations; and microradiography and computerised tomography scans of lungs with contrast injected vasculature. The major lesions were multiple, separate and coalescing foci of moderately proliferative small airway disease accompanied by intense neovascularisation of the bronchial circulation. As a result of bronchial artery angiogenesis, the systemic circulation dominated the vascular supply of the air exchange structures in affected areas, producing an apparent left to right shunt. Extensive areas of sequestered haemosiderophages indicated previous haemorrhage from vessels apparently supplied by the bronchial arteries. Diffuse and focal parenchymal destruction and connective tissue reactions in affected areas were considered to be secondary to localised haemorrhage and macrophage-induced damage. The aetiology of EIPH was not determined, but the multifocal, small airway-centred lesions indicated that low grade bronchiolitis, possibly of viral origin, was a factor. Gravitational effects also appear to contribute to dorsal distribution of the lesions. The mild focal and subclinical lesions confined to secondary lobules are thought to evolve into the serious lung pathology observed in EIPH cases through the effects of localised hypoxia induced by maximal exercise and partial airway obstruction. Once initiated, a vicious cycle of increasing inflammatory damage and further local bleeding is set in motion.

Animals↗
PubMed1987

Ozone-induced adaptive and reactive cellular changes in respiratory bronchioles of bonnet monkeys.

To characterize the response of respiratory bronchioles (RBs) to chronic high ambient levels of ozone, bonnet monkeys were exposed for 90 days to 0, 0.4, or 0.64 ppm ozone (UV photometric standard; 3 monkeys/exposure). Morphologic changes in respiratory bronchiolar epithelium and interstitium were evaluated quantitatively at both the light and transmission electron microscopic levels. Significant changes in respiratory bronchioles following exposure included: a thicker wall and a narrower lumen, a thicker epithelial compartment and a much thicker interstitial compartment, shifts in epithelial cell populations with many more nonciliated bronchiolar epithelial cells and fewer squamous type I epithelial cells, larger nonciliated bronchiolar epithelial cells with a larger complement of cellular organelles associated with protein synthesis, greater amounts of both interstitial fibers and amorphous ground substance, greater numbers of interstitial smooth muscle cells per epithelial basal lamina surface area, and greater volumes of interstitial smooth muscle, macrophages, mast cells, and neutrophils per epithelial basal lamina surface area. These observations imply that chronic ozone exposure causes a concentration-dependent reactive peribronchiolar inflammatory response and an adaptive response consisting of hypertrophy and hyperplasia of the nonciliated bronchiolar cell.

Adaptation, Physiological↗
PubMed1985

Structural evaluation of the respiratory system.

The theoretical and practical bases for morphological evaluation of the respiratory system useful for inhalation toxicology are reviewed. For most studies we recommend a comprehensive gross examination followed by in vitro tracheal infusion of a fixative containing both glutaraldehyde and formaldehyde in cacodylate buffer. Lungs fixed in this manner are suitable for LM, SEM, and TEM and lung volumes can be determined. The airway orientation of many lesions and the potential for gradients of damage are considered in the lung sampling plan. While LM of paraffin sections continues to be the basic method for evaluation, the SEM and TEM, especially when ancillary methods are used, provide valuable additional information. The use of backscattered electrons and energy-dispersive X-ray analysis in the SEM provides information concerning the localization and elemental analyses of particles. Cytochemical procedures characterize biological activities of specific cell types and are becoming more widely used. Morphometry permits correlation of quantified structure with physiological and biochemical data.

Animals↗
PubMed1985

Respiratory bronchiolitis following long-term ozone exposure in bonnet monkeys: a morphometric study.

To quantitate the response of respiratory bronchiolar (RB) epithelium and peribronchiolar connective tissue (PCT) to chronic exposure to high ambient levels of ozone, two groups of 8 adult male bonnet monkeys each were subjected 8 h daily for one year to 0.64 ppm (UV standard) ozone or filtered air, respectively. Blocks of tissue selected throughout the lung and from first generation RBs following airway microdissection had the following significant exposure-related changes: 57% greater volume of RB in the lung, 27% smaller diameter of RB lumen, 179% thicker media and intima of peribronchiolar arterioles, 61% thicker RB epithelium, and 77% thicker PCT. The increase in thickness of the RB wall resulted primarily from an 84% increase in PCT, with the remainder from the epithelium. Estimates of cellular numerical density showed an 81% increase in cuboidal bronchiolar cells and an 87% decrease in type 1 pneumocytes in the exposed group. Cell volumes from serial section reconstruction showed significantly larger cuboidal bronchiolar (79%), ciliated (117%), and type 2 (66%) cells over controls. Significant PCT changes included more amorphous extracellular matrix (288%), neutrophils (1523%), and lymphocytes/plasma cells (307%). The number of fibroblasts and the volume of extracellular fibers were larger than control values by 44% and 31% in the exposed group, but these changes were not statistically significant. Centriacinar changes due to exposure to long-term, high ambient ozone in bonnet monkeys results in narrowing of respiratory bronchioles primarily by peribronchiolar inflammation (inflammatory cells, fibers, amorphous matrix) and secondarily through hyperplasia of cuboidal bronchiolar cells.

Animals↗
PubMed1984

Long-term consequences of exposure to ozone. I. Lung collagen content.

Lung collagen content of rats and monkeys (Macaca fascicularis) exposed to ozone for 1 to 13 weeks and for 1 year, respectively, was quantified by measurement of 4-hydroxyproline in hydrolysates of whole lungs. In addition, ratios of type I to type III collagen in the lungs of the same monkeys were also evaluated by cyanogen bromide peptide mapping techniques. We observed elevated levels of collagen in lungs of both species of animals exposed to ozone. We conclude that elevations in collagen synthesis rates in lungs of rats and monkeys acutely exposed to high levels of ozone are reflected by corresponding increases in lung collagen content over subchronic and chronic time frames. Preliminary results on young rats also suggest that removal of rats from atmospheres containing ozone does not cause reversal of such increases in lung collagen content. To the contrary, recovery periods of up to 6 weeks seem to exacerbate the observed increases in lung collagen content.

Animals↗
PubMed1984

How to cheat in morphology: the renal ultrafilter.

It is easy to distort the "truth" in morphological reports in order to confirm a previously established dogma by selecting from a field of view only such details which are in accordance with the dogma and by ignoring parts contradictory to it. The renal corpuscle is used in this paper as an example and as a guide to the readers for future fraud.

Animals↗
PubMed1983

Comparative subgross anatomy of lungs. Pleuras, interlobular septa, and distal airways.

There are major species differences in the subgross anatomy of lungs that influence lung function and the reaction to injury. Variations in lobation and in the structure of pulmonary pleuras, interlobular septums, and distal airways are reviewed and tabulated. Thick pleura is usually accompanied by extensive interlobular connective tissue that forms complete interlobular septums in some species but only incomplete septums in others, resulting in functional differences. In some species, terminal bronchioles end by forming respiratory bronchioles, which in turn form alveolar ducts, whereas in other species terminal bronchioles end by directly forming alveolar ducts, resulting in species differences in acini. The methods used and the biological significance are discussed.

Animals↗
PubMed1983

Morphometry of in situ and lavaged pulmonary alveolar macrophages from control and ozone-exposed rats.

Effects of ambient levels of ozone on cell size and compartments were determined morphometrically for both in situ and lavaged pulmonary alveolar macrophages from rats exposed to filtered air or to filtered air with 0.60 ppm ozone. The ozone exposure was 8 hr/day for 3 days. Significant exposure-related compartmental volume density changes of in situ centriacinar macrophages were: decreased endoplasm (p less than 0.01); increased lysosome-like structures (p less than 0.01); decreased primary lysosomes (p less than 0.01); increased small and large secondary lysosomes (p less than 0.001); and decreased phagosomes/autophagosomes (p less than 0.05). In lavaged macrophages, the only significant exposure-related change was an increase in the density of large secondary lysosomes (p less than 0.01). Mean profile areas of in situ centriacinar macrophages from control and exposed rats were 86.94 micrometers2 and 112.04 micrometers2, respectively. The average mean cell volume V and mean caliper diameter D of macrophages lavaged from control rats were 1128.45 micrometers3 and 12.92 micrometers, respectively, whereas those from exposed rats were 1583.08 micrometers3 and 14.46 micrometers, respectively. Exposure-related increases in cell size were seen in both in situ and lavaged macrophages, but more significant differences in cell compartments were seen in the in situ centriacinar macrophages. Morphometry of pulmonary alveolar macrophages after ambient levels of ozone indicated increased uptake, storage, or both rather than cell damage. Comparison of in situ centriacinar and lavaged macrophages from both control and exposed rats revealed significant differences in their volume fractions of nucleus, cytoplasm, ectoplasm, mitochondria, lysosome-like structures, lipid droplets, vacuoles, and phagosome/autophagosomes. These differences between centriacinar and lavaged macrophages indicate different cell populations are sampled by these two methods.

Animals↗
PubMed1980

Acute respiratory bronchiolitis: an ultrastructural and autoradiographic study of epithelial cell injury and renewal in rhesus monkeys exposed to ozone.

The pathogenesis of acute respiratory bronchiolitis was examined in rhesus monkeys exposed to 0.8 ppm ozone fpr 4--50 hours. Epithelial injury and renewal was qualitatively and quantitatively characterized by correlated techniques of scanning and transmission electron microscopy as well as by light-microscopic autoradiography following labeling with tritiated thymidine. Extensive degeneration and necrosis of Type 1 epithelial cells occurred on the respiratory bronchiolar wall during the initial 4--12 hours of exposure. Increased numbers of labeled epithelial cells were present in this region after 18 hours of exposure, and the highest labeling index (18% was measured after 50 hours of exposure. Most (67--80%) of the labeled cells and all the mitotic epithelial cells (22) observed ultrastructurally were cuboidal bronchiolar epithelial cells. Of the labeled epithelial cells, 20--33% were Type 2 epithelial cells. After 50 hours of exposure the respiratory bronchiolar epithelium was hyperplastic. The predominant inflammatory cell in respiratory bronchiolar exudate was the alveolar macrophage. Monkeys that were exposed for 50 hours and allowed to recover in unozonized air for 7 days had incomplete resolution of respiratory bronchiolar epithelial hyperplasia. The results indicate that Type 1 epithelial cells lining respiratory bronchioles are the cell type most sensitive to injury and that both cuboidal bronchiolar epithelial cells and Type 2 epithelial cells function as stem cells in epithelial renewal.

Acute Disease↗
PubMed1978

A comparative study of cell renewal after exposure to ozone or oxygen. Response of terminal bronchiolar epithelium in the rat.

Cell renewal patterns of the terminal bronchiolar epithelium of rats were examined during 7-day exposures to either 0.8 ppm of ozone or 80 per cent O2. Terminal bronchiolar epithelial cells were classified and counted in ciliated, nonciliated secretory (Clara), and nonciliated, nonsecretory categories. Thymidine labeled with hydrogen-3 was used in conjunction with light microscopic autoradiography to obtain labeling indices in exposed rats at 6, 24, 72, and 168 hours compared to control rats at 6 and 168 hours. Results indicated that both ozone and O2 initiated a proliferative response of terminal bronchiolar epithelium, but that the response to O2 insult was delayed in onset and of lesser magnitude. Most importantly, the differential cell counts revealed that nonciliated secretory cells were the primary proliferating cell type at all periods after oxidant insult. This proliferative response continued with persistence of the insult through 168 hours. Shifts in proportions of cell types and labeling indices during exposure supported the view that nonciliated secretory cells are the reparative bronchiolar cells and that new ciliated cells are mainly derived from them.

Animals↗
PubMed1977

Morphometry of the distal air spaces in lungs of aging dogs.

Changes in pulmonary morphometric measurements with age were examined by manual and automated methods in 14 normal beagle dogs aged 289-3,694 days. The study was instituted as a statistical adjunct to previous morphological studies on these dogs that showed anthracosis and associated dilatations in the distal airways in aged dogs. With increasing age, the volumetric density of alveolar ducts increased concomitantly with decreases in the volumetric densities of alveoli and alveolar parenchymal tissue. The numerical and surface densities of alveoli also decreased with age. A comparison of an automated method with accepted manual methods showed no significant differences in stereological measurements of the distal air spaces with the exception of an overestimation of surface density by the automated method. The automated method was found to be a satisfactory method for evaluating the relative differences in alveolar surface densities and the volumetric densities of respiratory air space and parenchymal tissue.

Aging↗