Effects of sulfur dioxide or ammonium sulfate exposure, alone or combined, for 4 or 8 months on normal and elastase-impaired rats

Smith, L.G.; Busch, R. H.; Buschbom, R.L.; Cannon, W.C.; Loscutoff, S.M.; Morris, James E.

doi:10.1016/s0013-9351(89)80022-2

Cited by 4 publications

(2 citation statements)

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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). However, in the guinea pig model of elastase-induced emphysema, exposure to ammonium sulfate aerosol resulted in more pronounced lung functional changes (88), suggesting that interactive effects may be species dependent.…”

Section: Genetically Derived Models Ofmentioning

confidence: 87%

“…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: Genetically Derived Models Ofmentioning

confidence: 99%

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Rodent models of cardiopulmonary disease: their potential applicability in studies of air pollutant susceptibility.

Kodavanti

Costa

Bromberg

1998

Environ Health Perspect

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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.ImagesFigure 2

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