Pulmonary response to exposure to ozone of emphysematous rats

Yokoyama, Eiji; Nambu, Ziro; Ichikawa, Isamu; Uchiyama, Iwao; Arakawa, Hatsuko

doi:10.1016/s0013-9351(87)80012-9

Cited by 11 publications

(6 citation statements)

References 10 publications

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“…The depression of TLC was greatest on day 3 but still apparent on day 5. Residual volume was increased after a single 23-h exposure, similar to that reported by Yokoyama et al (35) for rats exposed to 1.0 ppm O 3 for 24 h. At Cold and Room T a levels, RV returned to control levels by day 2 and was no longer affected by O 3 . However, at Warm T a , RV dropped below baseline levels with either Continuous or Intermittent exposure.…”

supporting

confidence: 87%

Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters

Wiester

Watkinson

Costa

et al. 1996

Journal of Applied Physiology

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Pulmonary toxicity of ozone (O3) was examined in adult male Fischer 344 rats exposed to 0.5 parts/million O3 for either 6 or 23 h/day over 5 days while maintained at an ambient temperature (Ta) of either 10, 22, or 34 degrees C. Toxicity was evaluated by using changes in lung volumes and the concentrations of constituents of bronchoalveolar lavage fluid that signal lung injury and/or inflammation. Results indicated that toxicity increased as Ta decreased. Exposures conducted at 10 degrees C were associated with the greatest decreases in body weight and total lung capacity and the greatest increases in lavageable protein, lysozyme, alkaline phosphatase activity, and percent neutrophils. O3 effects not modified by Ta included increases in residual volume and lavageable potassium, glucose, urea, and ascorbic acid with exposure at 34 degrees C. Most effects were attenuated during the 5 exposure days and/or returned to normal levels after 7 air recovery days, regardless of prior O3 exposure or Ta. It is possible that Ta-induced changes in metabolic rate may have altered ventilation and, therefore, the O3 doses among rats exposed at the three different Ta levels.

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supporting

confidence: 87%

Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters

Wiester

Watkinson

Costa

et al. 1996

Journal of Applied Physiology

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“…Sixty days of O 3 exposure in rats with BLM-induced pulmonary damage did not further increased either the intensity of pulmonary damage or the frequency of bronchopneumonia. Similarly, a lack of synergism between O 3 exposure and previous lung damage has been reported in rats with elastase-induced pulmonary emphysema (Yokoyama et al, 1987). Sequence of O 3 exposure could be determinant.…”

Section: Long-term Ozone Exposurementioning

confidence: 79%

“…Because individuals with chronic lung disease are a high-risk group for the effects of air pollutants (Bascom, 1996;Oyarzún et al, 1998), experimental animal models of pulmonary emphysema (Yokoyama et al, 1987) and airway inflammation (Last et al, 2004) have been used to study the effects of ozone (O 3 ). Another suitable model may be bleomycin-induced pulmonary fibrosis (F-BLM) in rats (Dussaubat et al, 1995, Cooper 2000, Borzone et al, 2001.…”

Section: Introductionmentioning

confidence: 99%

Effect of 0.25 ppm Ozone exposure on pulmonary damage induced by bleomycin

2005

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To study the effect of ozone in a chronically damaged lung, we used a bleomycin (BLM) induced pulmonary fibrosis model. Both endotracheal instillation of BLM and O 3 exposure both produce lung inflammation and fibrosis. Oxidative stress would be a common mechanism of damage for both BLM and O 3. Our aim was to assess lung injury induced by 5 and 60 days of intermittent exposure to 0.25 ppm O 3 in rats with bleomycininduced pulmonary fibrosis. Thirty-day-old Sprague Dawley rats were endotracheally instilled with BLM (1 U/100 g body weight) and, 30 days later, exposed to 0.25 ppm O 3 (0.25 ppm 4 h per day, 5 days a week). Histopatology controls were instilled with saline and breathing room air. Histopathological evaluation of lungs was done 5 and 60 days after O 3 exposure. BLM-induced lung damage did not change after 60 days of intermittent O 3 exposure. Five days of O 3 exposure increased the mean score of BLM-induced pulmonary inflammation and fibrosis (p=0.06). Frequency of bronchopneumonia increased from 1/7 to 6/6 (p <0.001), suggesting that a short-term exposure to O 3 in a previously damaged lung might be a risk factor for developing further lung injury.

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“…In the hamster and rat models of elastase-induced emphysema, exposure to hyperoxia, 03, or a mixture of olefin-03-SO2 reaction products did not Environmental Health Perspectives * Vol 106, Supplement 1 * February 1998 reveal unusual susceptibility in terms of the resulting pulmonary inflammation and lung dysfunction (86,90,92). Similarly, SO2 or ammonium sulfate did not affect emphysematous rats pretreated with elastase any differently than normal rats (91).…”

Section: Rodent Models Of Cardiopulmonary Diseases Pulmonary Diseasesmentioning

confidence: 98%

“…A number of studies have been conducted that examine susceptibility of emphysematous animals to inhaled pollutants (77,(86)(87)(88)(89)(90)(91). In the hamster and rat models of elastase-induced emphysema, exposure to hyperoxia, 03, or a mixture of olefin-03-SO2 reaction products did not Environmental Health Perspectives * Vol 106, Supplement 1 * February 1998 reveal unusual susceptibility in terms of the resulting pulmonary inflammation and lung dysfunction (86,90,92).…”

Section: Rodent Models Of Cardiopulmonary Diseases Pulmonary Diseasesmentioning

confidence: 99%

Rodent Models of Cardiopulmonary Disease: Their Potential Applicability in Studies of Air Pollutant Susceptibility

Kodavanti¹,

Costa²,

Bromberg³

1998

Environmental Health Perspectives

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The mechanisms by which increased mortality and morbidity occur in individuals with preexistent cardiopulmonary disease following acute episodes of air pollution are unknown. Studies involving air pollution effects on animal models of human cardiopulmonary diseases are both infrequent and difficult to interpret. Such models are, however, extensively used in studies of disease pathogenesis. Primarily they comprise those developed by genetic, pharmacologic, or surgical manipulations of the cardiopulmonary system. This review attempts a comprehensive description of rodent cardiopulmonary disease models in the context of their potential application to susceptibility studies of air pollutants regardless of whether the models have been previously used for such studies. The pulmonary disease models include bronchitis, emphysema, asthma/allergy, chronic obstructive pulmonary disease, interstitial fibrosis, and infection. The models of systemic hypertension and congestive heart failure include: those derived by genetics (spontaneously hypertensive, Dahl S, renin transgenic, and other rodent models); congestive heart failure models derived by surgical manipulations; viral myocarditis; and cardiomyopathy induced by adriamycin. The characteristic pathogenic features critical to understanding the susceptibility to inhaled toxicants are described. It is anticipated that this review will provide a ready reference for the selection of appropriate rodent models of cardiopulmonary diseases and identify not only their pathobiologic similarities and/or differences to humans but also their potential usefulness in susceptibility studies.

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Pulmonary response to exposure to ozone of emphysematous rats

Cited by 11 publications

References 10 publications

Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters

Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters

Effect of 0.25 ppm Ozone exposure on pulmonary damage induced by bleomycin

Rodent Models of Cardiopulmonary Disease: Their Potential Applicability in Studies of Air Pollutant Susceptibility

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