RODENT MODELS OF CARDIOPULMONARY DISEASE - THEIR POTENTIAL APPLICABILITY IN STUDIES OF AIR POLLUTANT SUSCEPTIBILITY

Citation
Up. Kodavanti et al., RODENT MODELS OF CARDIOPULMONARY DISEASE - THEIR POTENTIAL APPLICABILITY IN STUDIES OF AIR POLLUTANT SUSCEPTIBILITY, Environmental health perspectives, 106, 1998, pp. 111-130
Citations number
315
Categorie Soggetti
Public, Environmental & Occupation Heath","Environmental Sciences
ISSN journal
00916765
Volume
106
Year of publication
1998
Supplement
1
Pages
111 - 130
Database
ISI
SICI code
0091-6765(1998)106:<111:RMOCD->2.0.ZU;2-C
Abstract
The mechanisms by which increased mortality and morbidity occur in ind ividuals with preexistent cardiopulmonary disease following acute epis odes of air pollution are unknown. Studies involving air pollution eff ects on animal models of human cardiopulmonary diseases are both infre quent and difficult to interpret. Such models are, however, extensivel y used in studies of disease pathogenesis. Primarily they comprise tho se developed by genetic, pharmacologic, or surgical manipulations of t he cardiopulmonary system. This review attempts a comprehensive descri ption of rodent cardiopulmonary disease models in the context of their potential application to susceptibility studies of air pollutants reg ardless of whether the models have been previously used for such studi es. The pulmonary disease models include bronchitis, emphysema, asthma /allergy, chronic obstructive pulmonary disease, interstitial fibrosis , and infection. The models of systemic hypertension and congestive he art failure include: those derived by genetics (spontaneously hyperten sive, Dahl S, renin transgenic, and other rodent models); congestive h eart failure models derived by surgical manipulations; viral myocardit is; and cardiomyopathy induced by adriamycin. The characteristic patho genic features critical to understanding the susceptibility to inhaled toxicants are described. It is anticipated that this review will prov ide a ready reference for the selection of appropriate rodent models o f cardiopulmonary diseases and identify not only their pathobiologic s imilarities and/or differences to humans but also their potential usef ulness in susceptibility studies.