Avian Pathology PDF - The Pathology of Normobaric Oxygen Toxicity in Budgerigars

Avian Pathology ISSN: 0307-9457 (Print) 1465-3338 (Online) Journal homepage: www.tandfonline.com/journals/cavp20 The pathology of normobaric oxygen toxicity in budgerigars (Melopsittacus undulatus) Susan M. Jaensch, L. Cullen & S. R. Raidal To cite this article: Susan M. Jaensch, L. Cullen & S. R. Raidal (2001) The pathology of normobaric oxygen toxicity in budgerigars (Melopsittacus undulatus), Avian Pathology, 30:2, 135-142, DOI: 10.1080/0307945012004453 To link to this article: https://doi.org/10.1080/0307945012004453 Published online: 17 Jun 2010. Submit your article to this journal Article views: 324 View related articles Full Terms & Conditions of access and use can be found at https://www.tandfonline.com/action/journalInformation?journalCode=cavp20 Avian Pathology ( 2001 ) 30, 135– 142 The pathology of normobaric oxygen toxicity in budgerigars ( Melopsittacus undulatus ) Susan M. Jaensch*, L. Cullen & S. R. Raidal Murdoch University, Division of Veterinary and Biomedical Sciences, South Street, Murdoch, WA 6150, Australia The effects of normobaric oxygen exposure were investigated in budgerigars ( Melopsittacus undulatus ). Sixty birds were randomly divided into four equal groups of 15. These groups were randomly allocated as control, acute exposure, repeated acute exposure or chronic exposure. Control birds were exposed to 72 continuous hours of 21% oxygen in a sealed, enclosed chamber. Acute exposure, repeated acute exposure and chronic exposure groups were exposed oxygen at minimum concentration of 95% for a single 3-h period, a 3-h period daily for three sequential days, or a single 72-h period in a sealed, enclosed chamber, respectively. Oxygen exposure resulted in significant alteration in the histological morphology of respiratory exchange tissue, with severe oedema, and inflammatory cell infiltration. Electron micrographs revealed thickening of the blood– gas barrier with the tissue harmonic thickness increasing from 226 ± 90 nm in control birds to 639 ± 393 nm following repeated acute exposure, with the total harmonic thickness increasing from a control value of 345 ± 146 nm to 837 ± 423 nm at the same time. Chronic oxygen exposure resulted in significant changes in cell morphology including thickening of endothelial cells, ruffling of type I respiratory endothelial cells and interstitial vacuolation. These results indicate that budgerigars undergo significant morphological and ultra- structural changes in respiratory exchange tissue following exposure to 100% oxygen. Introduction associated with either acute or chronic oxygen exposure. Oxygen therapy is common in avian In mammals, exposure to normobaric oxygen medicine, either as part of inhalant anaesthesia concentrations greater than 95% results in pulmo- administration or as an adjunct to medical support- nary oxygen toxicity, with inflammatory changes ive care. As such, the role of oxygen stress and apparent after acute exposure ( Davis et al., 1983 ). oxygen toxicity in these situations is of clinical With more prolonged exposure, progressive chan- importance. ges ultimately result in death ( Crapo et al., 1980; Previous research in our laboratory has described Davis et al., 1983; Padmanabhan et al., 1985; Ward the enzymatic and non-enzymatic antioxidant res- et al., 1986; Barazzone et al., 1998; Johnston et al., ponses to normobaric hyperoxia in budgerigars 1998 ). Chronic hyperoxic exposure is associated ( Melopsittacus undulatus ) ( Jaensch et al., 2001a/b). with the initiation of inflammatory and destructive Significant reduction in the concentrations of sev- processes, ultimately resulting in severe disruption eral non-enzymatic antioxidants including uric acid, of the blood– gas barrier with hypertrophy of tocopherols and carotenoids, and elevations of both endothelial cells and necrosis of type I pneumocytes blood and pulmonary concentrations of glutathion e ( Crapo et al., 1980). with chronic oxygen exposure in comparison with In birds, the clinical and visible pathological controls indicated progression from oxygen stress changes associated with prolonged normobaric to oxygen toxicity. The present paper describes the hyperoxic exposure have been reported ( Stauber et morphological changes associated with acute and al., 1991 ). However, there are no reports describ- chronic normobaric hyperoxic exposure in ing the histological and ultra-structural changes budgerigars. * To whom correspondence should be addressed. E-mail: [email protected] u Received 27 June 2000. Accepted 30 September 2000. ISSN 0307-9457 ( print)/ISSN 1465-3338 ( online)/01/020135-0 8 © 2001 Houghton Trust Ltd DOI: 10.1080/0307945012004453 136 S. M. Jaensch et al. Materials and Methods addition, the intercept lengths of the total exchange barrier were measured along the test lines as previously described ( Weibel et al., Animals and exposure conditions 1993 ). The harmonic mean thicknesses were calculated for each Sixty budgerigars aged 12 to 36 months sourced from a single aviary component of the gas exchange barrier as previously described ( Vitali, flock were used in the study. Prior to and following exposure, the birds 1996 ) with plasma barrier thicknesses grouped by class. were held in breeding cages with four birds per cage under a 12-h light To count cell populations, each electron micrograph was placed regime. The birds were randomly divided into four equal groups each under an unbiased counting frame and nuclei profiles within the frame of 15 birds, which were allocated as control, acute, repeated acute and characterized and counted. To remove bias, a counting rule previousl y chronic exposure groups. described was used ( Gundersen et al., 1988 ). This involved the Oxygen exposure was performed in a clear 260 l perspex chamber inclusion of nuclei within the frame or touching the boundaries of the with the birds’ normal diet and water available ad libitum. A single frame but not intersecting the full drawn exclusion edges or their oxygen inflow was situated at the base of one end of the chamber, and extensions. a single outflow was situated at the top of the opposite end. The oxygen concentration of outflowing gas from the chamber was measured by a Statistical analysis Hudson Ventronics 5577 oxygen analyzer, utilizing a galvanic assay and corrected for temperature ( Hudson Ventronics Division, Temecula, Comparison between groups was performed by analysis of variance CA, USA). Initial oxygen flow rates of 15 l/min were maintained until with comparison of means by Tukey tests, and between pairs of data by the oxygen concentration of outflowing gas reached 95%, which was unpaired Students t tests. Data were considered significant when P < maintained throughout the exposure by flow rates of 6 to 15 l/min as 0.05. All statistical analysis was performed using the SigmaStat required. Control birds were exposed to 3 days of air ( 21% O2 ) statistical analysis program ( SPSS, Chicago, IL, USA). delivered from a cylinder at similar flow rates within the chamber. Acute exposure, repeated acute exposure and chronic exposure groups were exposed to oxygen for a single 3-h period, a 3-h period daily for three sequential days, or a single 72-h period, respectively. For each Results group, five randomly selected birds were euthanased immediately after the end of oxygen exposure, five birds were euthanased 24 h after The birds in the acute and repeated acute expo- exposure and the remaining five birds 96 h after exposure. sure groups showed no clinical evidence of depression or respiratory distress. Birds from the Sample collection chronic exposure group were clinically normal Euthanasia was performed by briefly anaesthetizing each bird with during the oxygen exposure and for 12 h after halothane ( Halothane, Merial Australia Pty Ltd, Parramatta, Australia) exposure. However, 24 h after exposure, about six in oxygen and exsanguination by jugular venipuncture using a 25 G ´ of the remaining 10 birds in this group showed 5/8 inch needle on a 3 ml syringe. Following exsanguination, the lungs were collected and washed with ice-cold 0.9% sodium chloride evidence of respiratory distress. Two of these solution. The caudal aspect of each lung was collected for histology birds died as they were being captured, and and transmission electron microscopy. postmortem examination of these birds revealed bilaterally symmetrical, severe pulmonary conges- Histopathology tion and oedema. Consequently, all remaining From each bird, one portion of lung was collected into 10% buffered birds were immediately euthanased and necro- formalin and processed for histological examination. The tissue was psied, and similar lesions were found in all of embedded in paraffin blocks, and 10 m m sections cut and stained with these birds. haematoxylin and eosin using standard procedures for light micro- scopic sections. One section from each bird was blindly scored for congestion, haemorrhage, oedema, haemosiderin, heterophils, macro- Histological studies phages and flattening of atria, with subjective scoring of 0 to 3 for each parameter, with 0 being normal and 3 severe change. Histological changes were minimal following acute and repeated acute exposures. Following chronic Transmission electron microscopy exposure, there was evidence of mild pulmonary congestion, moderate pulmonary oedema centred Freshly collected lung tissue for transmission electron microscopy was cut into 1 mm cubes in ice-cold 2% glutaraldehyde, washed in on parabronchi, mild heterophilic bronchitis and Sorensen’s phosphate buffer, postfixed in 2% osmium tetroxide, bronchial epithelial hyperplasia. These changes are dehydrated in a graded series of alcohols and embedded in TAAB demonstrated in Figure 1. Epon. One micrometre sections were cut with a glass knife and stained Histological scores were evaluated by the day with toluidine blue. The region of interest was identified, trimmed and of euthanasia, and no significant differences were sectioned into 90 nm sections using a diamond knife. The sections were retrieved on 200 mesh uncoated copper grids and stained for 5 min with found between days, thus only data grouped by uranyl lead acetate and counter stained with lead citrate for 4 min for exposure period are presented in this paper. Histo- electron microscopic studies using a Philips CM 100 bio-transmission logical scores for congestion, haemorrhage, hae- electron microscope. For morphometric studies, a series of three mosiderin and atrial flattening were not signifi- electron micrographs of consecutive grid spaces were taken from the cantly different between exposure periods. first encountered area of exchange tissue of suitable quality for each bird. Electron micrographs were taken at 12 000´ magnification for Histological scores for oedema, heterophils and morphometric studies. A calibration grid was photographed with each macrophages were significantly elevated in the electron micrograph to allow accurate determination of chronic exposure group compared with the control magnification. group, but were not significantly elevated in either For determination of blood– gas barrier measurements, each electron acute exposure groups. Control scores for oedema, micrograph was placed under a randomly orientated plastic overlay that contained horizontal lines spaced 4 cm apart. The orthogonal intercept heterophils and macrophages were 0.33 ± 0.49, 0 lengths of both the tissue and plasma components of the gas exchange ± 0 and 0.20 ± 0.41, respectively, while chronic barrier were measured as previously described ( Mayhew, 1991). In exposure scores were 1.14 ± 1.17, 0.64 ± 0.75 and Avian pulmonary oxygen toxicity 137 ( A) ( B) Figure 1. Photomicrograph of parabronchi from a budgerigar in the control group ( A) and from a budgerigar following 72 h 100% O2 exposure ( B). The parabronchus from the latter budgerigar demonstrates pulmonary oedema, proteinaceous fluid and heterophil accumulation within the parabronchus, bronchial epithelial hyperplasia and sloughing of epithelial cells into the lumen. 0.93 ± 1.07, respectively. The total histologica l groups, but not compared with the control group. score, being the sum of all other histologica l Total histological scores were 6.13 ± 1.64, 1.80 ± scores for each individual, was significantly ele- 1.15, 2.00 ± 1.13 and 6.86 ± 4.85 after control, vated in the chronic exposure group compared acute, repeated acute and chronic exposure, with both the acute and repeated acute exposure respectively. 138 S. M. Jaensch et al. Figure 2. Electron micrograph of normal budgerigar pulmonary gas exchange tissue. Morphological studies increased respiratory epithelial type I and type II cells. These results are summarized in Figure 1. Data collected from control birds were not sig- Morphological changes of cells within the blood– nificantly different between days, and therefore gas barrier were apparent in electron micrographs of were pooled to provide control data for this study. birds from the chronic exposure group in comparison Mean harmonic thickness of the tissue barrier in with those from the control group. Figure 2 shows an control birds was 226 ± 90 nm. This was sig- electron micrograph from a control bird, with thin nificantly elevated immediately following repeated endothelial cell and epithelial cell walls and no acute exposure to 639 ± 393 nm. The harmonic evidence of interstitial vacuolation. The endothelial thickness of the tissue barrier was within normal cells, respiratory epithelial cells and interstitial space range at all other times. Mean control plasma all underwent significant morphological change barrier harmonic thickness was 45 ± 27 nm. Meas- following oxygen exposure, with the most sig- urements were within this range at all times after nificant change occurring following chronic oxygen each oxygen exposure. The control total barrier was exposure. Following chronic oxygen exposure, 345 ± 146 nm. All measurements were within the respiratory epithelial cells underwent morphological normal range except 24 h after acute exposure and changes, including formation of extensive ruffling of immediately after repeated acute exposure, when type I epithelial cells ( Figure 3). Changes in the total harmonic thickness was elevated to 640 ± endothelial cells were predominantly increased 257 and 837 ± 423 nm, respectively. thickness of endothelial cells resulting in constric- A total of 246 eligible nuclear profiles was tion of the capillary lumen ( Figure 4). Significant identified on the electron micrographs. Significant increased interstitial vacuolation was also evident changes in cell population were only found in following chronic oxygen exposure ( Figure 5). heterophils, with an increase from 0 ± 0 to 7.7 ± 15.8% of nuclei profiles between control and Discussion chronic exposure. Trends in cell population included a decrease in interstitial cells and respira- The changes demonstrated in both the histologica l tory epithelial type I cells, and an increase in and morphological studies of the birds in the current endothelial cells between the control and repeated study are consistent with changes described in acute exposure groups. Chronic exposure resulted mammals during progressive lethal oxygen toxicity. in trends of decreased endothelial cells, and In mammals, the inflammatory phase of lethal Avian pulmonary oxygen toxicity 139 Figure 3. Electron micrograph of pulmonary gas exchange tissue following 72 h 100% O2 exposure. Arrowheads indicate areas of respiratory epithelial cell ruffling. Other changes include vacuolation of endothelial cells. oxygen toxicity results in endothelial cell ultra- In mammalian models of oxygen toxicity, injury structural changes, associated with peri-capillary and death of endothelial cells, resulting in massive accumulation of fluid. In addition, there is an leakage of fluid and its accumulation in alveoli, is increase in platelets within capillaries and an considered to be a major cause of respiratory failure associated increase in heterophils in the inter- and mortality ( Barazzone et al., 1998 ). Endothelial stitium. The destructive phase primarily results in cell damage has been reported to precede respira- destruction of endothelial cells, with further increa- tory epithelial cell damage in oxygen toxicity ses in heterophils and no significant changes in the ( Jenkinson, 1982) both due to the close proximity to numbers of respiratory epithelial type I and type II elevated oxygen partial pressure and thus poten- cells ( Crapo, 1986). In the current study, there were tially increased production of reactive oxygen no significant changes associated with acute expo- species, and secondarily due to aggregation and sure, but changes associated with repeated acute migration of inflammatory cells through the capil- oxygen exposure included elevation in the percen- lary walls ( Jenkinson, 1982; Davies, 1991). tages of endothelial cells and heterophils, and Although evidence of endothelial cell injury was thickening of both the tissue barrier and total gas present in the morphological studies, extravascular exchange barrier. The severe oedema, increased leakage of fluid into air capillaries was not seen. inflammatory cells and decreasing numbers of Indeed, most extravascular fluid was identified endothelial cells associated with chronic exposure surrounding and within parabronchi. This is in are consistent with the destructive phase of oxygen contrast with previously reported lesions in mam- toxicity. Differentiation of these two major phases mals ( Crapo et al., 1978, 1980; Ainsworth et al., of lethal oxygen toxicity is shown in Figure 1. 1986 ), where oedema occurred predominantly in Despite the apparent severity of these lesions, the the alveolar spaces. In the current study, it is distribution of the lesions was variable, with possible that the oedema in the parabronchi may apparently severely affected parabronchi sometimes still result in obstruction of gas flow; however, this located immediately adjacent to histologically nor- change would have to be extensive to result in mal parabronchi. respiratory failure, due to the highly anastomosing 140 S. M. Jaensch et al. Figure 4. Electron micrograph of pulmonary gas exchange tissue following 72 h 100% O2 exposure. The arrowhead indicates a blood capillary with a dramatically thickened wall resulting in constriction of the capillary lumen. The surrounding capillaries show some evidence of vacuolation of endothelial cell cytoplasm. Figure 5. Electron micrograph of pulmonary gas exchange tissue following 72 h 100% O2 exposure. Arrowheads indicate areas of respiratory endothelial cell ruffling. Arrows indicate interstitial vacuolation. Avian pulmonary oxygen toxicity 141 nature of the air capillary network ( Fedde, 1986). diately following repeated acute exposure, while Accumulation of inflammatory cells, both hetero- total barrier thickness was significantly increased phils and macrophages, within oedema fluid after only at 24 h after acute exposure and immediately both repeated acute and chronic exposures provides following repeated acute exposure. In this study, in supporting evidence of endothelial cell damage. contrast to previous mammalian studies, oedema Of all the cells that comprise pulmonary tissue, around the areas of gas exchange was not a major respiratory epithelial cells are exposed to the feature of the pathological changes found. The highest oxygen partial pressures and this results in a accumulation of both oedema and inflammatory high risk of cellular injury during periods of cells were most prominent within parabronchi. The hyperoxia. In addition, respiratory epithelial type I increase in barrier thickness following repeated cells have a limited capacity to recover or regen- acute exposure may be associated with the trend to erate following injury; thus, once damaged, they an increased percentage of endothelial nuclei, rely on respiratory epithelial type II cells to possibly reflecting rounding up and proliferation of recolonize areas of denuded basement membrane this cell type in response to the repeated oxidative ( Davies, 1991). In the current study, there was no stress. Following chronic exposure, there was a significant change in epithelial type I cell popula- trend to a decreasing percentage of endothelial tion density after oxygen exposure. This is con- cells, possibly reflecting death of this cell type, a sistent with previous mammalian studies in which principal cell in the tissue barrier component. no significant change in this population occurred Despite a lack of significant increase in tissue or following 60 h exposure to 100% O2 ( Crapo et al., total barrier thickness, respiratory function as 1980; Crapo, 1986). Nevertheless, there was evi- determined by blood gas analysis was significantl y dence of type I cellular damage in electron reduced in both repeated acute and chronic expo- micrographs following chronic exposure. Damage sure birds ( Jaensch et al., 2001a/b). This indicates to epithelial type I cells may result in exposure of that barrier thickness may be a poor indicator of respiratory basement membrane ( Davies, 1991), respiratory function in birds. resulting in activation and division of respiratory epithelial type II cells. This process was probably References occurring in chronically exposed birds, since there Ainsworth, D.M., Keith, I.M., Lobas, J.G., Farrell, P.M. & Eicker, S.W. was electron microscopic evidence of an increasing ( 1986 ). Oxygen toxicity in the infant rhesus monkey lung. Light population density of respiratory epithelial type II microscopic and ultrastructural studies. Histological Histopathology, cells at the expense of type I cells. 1, 75– 87. The control values for blood– gas barrier compo- Barazzone, C., Horowitz, S., Donati, Y.R., Rodriguez, I. & Piguet, P.-F. ( 1998 ). Oxygen toxicity in mouse lungs: pathways to cell death. nents in this study show some variation from American Journal of Respiratory Cell Molecular Biology, 19, previously reported values. The mean tissue barrier 573– 581. in the current study of 226 nm is higher than Crapo, J. D. ( 1986 ). Morphologic changes in pulmonary oxygen previously reported budgerigar values of 118 nm toxicity. Annual Review of Physiology, 48, 721–731. ( Dubach, 1981) and 117 nm ( Maina & King, 1982). Crapo, J.D., Peters-Golden, M., Marsh-Salin, J. & Shelburne, J.S. ( 1978 ). Pathologic changes in the lungs of oxygen-adapted rats. A Similarly, the mean plasma barrier of 45 nm is morphometric analysis. Laboratory Investigation, 39, 640– 653. higher than that previously reported in budgerigars Crapo, J.D., Barry, B.E., Foscue, H.A. & Shelburne, J. ( 1980 ). of 18 nm ( Dubach, 1981). These differences princi- Structural and biochemical changes in rat lungs occurring during pally reflect the different tissue fixation techniques exposure to lethal and adaptive doses of oxygen. American Review of used by the current and previous studies. Previous Respiratory Disease, 122, 123–143. Davies, P. ( 1991 ). Morphologic and morphometric techniques for the studies have used in situ instillation techniques to differentiation of drug- and toxin-induced changes in lung. Pharma- fix pulmonary tissue, resulting in possible disten- cological Therapeutics, 50, 321– 336. sion of gas capillaries with alterations in the Davis, W.B., Rennard, S.I., Bitterman, P.B. & Crystal, R.G. ( 1983 ). configuration of the blood gas barrier ( Davies, Pulmonary oxygen toxicity. Early reversible changes in human 1991 ). In the current study, tissue sampling require- alveolar structures induced by hyperoxia. The New England Journal ment for other areas of the study, including enzyme of Medicine, 309, 878– 883. Dubach, M. ( 1981 ). Quantitative analysis of the respiratory system of and metabolite assays, and priority given to the the house sparrow, budgerigar and violet eared hummingbird. maintenance of intra-alveolar and capillary cells, Respiration Physiology, 46, 43– 60. prevented the use of either infusion or perfusion Fedde, M.R. ( 1986 ). Respiration. In P.D. Sturkie ( Ed.), Avian fixation techniques. Physiology ( pp. 191–220). New York: Springer-Verlag. Gundersen, H.J.G., Bendtsen, T.F., Korbo, L., Macrussen, N., Moller, The inflammatory and destructive phases of A., Nielsen, K., Nyengaard, J.R., Pakkenberg, B., Sorensen, F.B., oxygen toxicity would be expected to result in Vesterby, A. & West, M.J. ( 1988 ). Some new, simple and efficient increased thickness of the blood– gas barrier both stereological methods and their use in pathological research and due to accumulation of cells and oedema fluid diagnosis. APMIS, 96, 379– 394. within the interstitial space and hypertrophy of the Jaensch, S., Cullen, L. & Raidal, S.R. ( 2001a ). Normobaric hyperoxic stress in budgerigars: enzymic antioxidants and lipid peroxidation. vascular endothelial cells ( Crapo et al., 1978, Comparative Biochemistry and Physiology C, 128( 2), 173–180. 1980 ). In the current study, the plasma barrier Jaensch, S., Cullen, L., Morton, L. & Raidal, S.R. ( 2001 ). Normobari c remained within the normal range at all times. The hyperoxic stress in budgerigars: non-enzymic antioxidants. Compar- tissue barrier was only significantly elevated imme- ative Biochemistry and Physiology C, 128( 2), 181–187. 142 S. M. Jaensch et al. Jenkinson, S.G. ( 1982 ). Pulmonary oxygen toxicity. Clinics in Chest ZUSAMMENFASSUNG Medicine, 3, 109–119. Die Pathologie der Toxizität von normobarem Sauerstoff bei Johnston, C.J., Stripp, B.R., Piedbeouf, B., Wright, T.W., Mango, G.W., Wellensittichen ( Melopsittacus undulatus ) Reed, C.K. & Finkelstein, J.N. ( 1998 ). Inflammatory and epithelial responses in mouse strains that differ in sensitivity to hyperoxic Die Effekte von normobarer Sauerstoffexposition wurden bei Well- injury. Experimental Lung Research, 24, 189– 202. ensittichen ( Melopsittacus undulatus ) untersucht. Sechzig Vögel Maina, J.N. & King, A.S. ( 1982 ). The thickness of the avian blood–gas wurden willkürlich in vier gleiche Gruppen von 15 aufgeteilt. Diese barrier: qualitative and quantitative observations. 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American Review of Respiratory abgedichteten, geschlossenen Raum einer Mindestkonzentration von Disease, 132, 164–167. 95% Sauerstoff ausgesetzt. Die Sauerstoffexposition führte zu einer Stauber, E., Krinke, M., Greene, S. & Wilkerson, M. ( 1991 ). Effects of signifikanten Veränderung der histologischen Morphologie des respir- increased concentration of inspired oxygen. Proceedings of the atorischen Austauschgewebes, mit starkem Ödem und entzündlicher European Chapter of the Association of Avian Veterinarians ( pp. Zellinfiltration. Elektronenmikroskopische Aufnahmen zeigten eine 104–114 ). Verdickung der Blut-Luft-Schranke mit einer Zunahme der harmo- Vitali, S. ( 1996 ). The functional morphology of the lungs of small nischen Gewebedicke von 226 ± 90 nm bei den Kontrolltieren auf 639 Australian passerines having different diurnal activity patterns. ± 393 nm nach der wiederholten akuten Exposition bei einer gleichzei- Ph.D. Thesis. Murdoch University, Perth. tigen Zunahme der harmonischen Gesamtdicke von einem Kon- Ward, P.A., Johnson, K.J. & Till, G.O. ( 1986 ). Animal models of trollwert von 345 ± 146 nm auf 837 ± 423 nm. Die chronische oxidant lung toxicity. Respiration, 50, 5–12. Sauerstoffexposition führte zu signifikanten Veränderungen der Zell- Weibel, E.R., Federspiel, W.J., Fryder-Doffey, F., Hsia, C.C.W., Konig, morphologie mit Verdickung der Endothelzellen, Kräuseln der Alveo- M., Stalder-Navarro, V. & Vock, R. ( 1993 ). Morphometric model for larzellen Typ I und Interstiumvakuolisierung. Diese Ergebnisse zeigen, pulmonary diffusing capacity 1. Membrane diffusing capacity. dass Wellensittiche im Anschluss an eine Belastung mit 100% Respiration Physiology, 93, 125–149. Sauerstoff erhebliche morphologische und ultrastrukturelle Veränder- ungen im respiratorischen Austauschgewebe durchmachen. RÉSUMÉ Toxicité de l’oxyg ène normobare chez des perruches ( Melopsittacus undulatus ) RESUMEN Les effets de l’exposition des perruches ( Melopsittacus undulatus ) à Patolog´õ a de la toxicidad normobárica de ox´õ geno en periquitos l’oxygène normobare ont été étudiés. Soixante oiseaux ont été répartis, ( Melopsittacus undulatus ) de façon aléatoire, en quatre groupes de 15 sujets et ont été soumis aux traitements suivants : – exposition forte, – exposition forte et répétée, Se investigaron los efectos de la exposición normob árica de ox´õ geno en – exposition chronique et – témoin non traité. Les groupes d’animaux periquitos ( Melopsittacus undulatus ). Se dividieron sesenta aves al azar ont été héberg és dans des chambres séparées, closes et scellées. Les en cuatro grupos iguales de 15 animales. Estos grupos se consideraron témoins ont été expos és durant 72 heures, en continu, à un taux como controles, exposición aguda, exposición aguda repetida y d’oxygène de 21 %. Les groupes : – exposé fortement, – exposé exposici ón crónica. Las aves control se expusieron durante 72 horas fortement et de façon répétée et – exposé de façon chronique ont été cont´õ nuas a un 21% de ox´õ geno en una cámara cerrada y sellada. Los soumis respectivement à un taux minimal en oxygène de 95 % durant grupos de exposición aguda, exposición aguda repetida y exposición : – une période de 3 heures ( une seule fois), – une période de 3 heures crónica fueron expuestos a una concentración m´õ nima del 95% de répétée trois jours de suite ou – une seule période de 72 heures. Cette ox´õ geno por un único periodo de 3 horas, a 3 horas diarias durante 3 exposition à l’oxygène a entraˆõ né des altérations significatives du d´õ as seguidos o a un periodo único de 72 horas respectivamente, en una parenchyme pulmonaire au niveau des zones d’échange avec beaucoup cámara cerrada y sellada. La exposición a ox´õ geno resultó en una d’œdème et une infiltration de cellules inflammatoires. En microscopie alteraci ón significativa de la morfolog´õ a microsc ópica del tejido de électronique, un épaississement de la membrane aérocapillaire a été intercambio respiratorio, con un edema severo y una infiltración con mis en évidence, l’épaisseur passant d’une valeur harmonique de 226 células inflamatorias. Las microfotograf´õ as electrónicas revelaron un ( 90 nm chez les témoins, à 639 ± 393 nm chez les animaux qui ont été aumento de grosor de la barrera sangre-gas con un aumento del grosor soumis à une exposition forte répétée, tandis que la moyenne harm ónico del tejido de 226 ± 90 nm. en las aves control hasta 639 ± harmonique totale a augmenté de 345 ± 146 nm à 837 ± 423 nm au 393 nm. en las aves que sufrieron una exposición aguda y repetida, con même moment. L’exposition chronique à l’oxygène a entraˆõ né des un incremento harmónico del grosor de un valor control de 345 ± lésions importantes au niveau de la morphologie des cellules, incluant 146 nm. hasta 837 ± 423 nm. en el mismo tiempo. La exposición un épaississement des cellules endothéliales, une ondulation des crónica al ox´õ geno resultó en cambios significativos en la morfolog´õ a cellules endotheliales respiratoires de type I et une vacuolisation celular incluyendo engrosamiento de las células endoteliales, retracción interstitielle. Ces résultats montrent que les perruches subissent des de las células endoteliales respiratorias de tipo I y vacuolización lésions morphologiques et ultrastructurales importantes au niveau des intersticial. Estos resultados indican que los periquitos padecen tissus des zones d’échange aérocapillaire suite à une exposition à un cambios morfológicos y ultraestructurales en el tejido respiratorio de taux d’oxygène de 100 %. intercambio cuando son expuestos a ox´õ geno al 100%.

Avian Pathology PDF - The Pathology of Normobaric Oxygen Toxicity in Budgerigars

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