You are here:
Rat Models of Cardiometabolic Diseases: Baseline Clinical Chemistries, and Rationale for their Use in Examining Air Pollution Health Effects
Citation:
Kodavanti, U., J. Russell, AND D. Costa. Rat Models of Cardiometabolic Diseases: Baseline Clinical Chemistries, and Rationale for their Use in Examining Air Pollution Health Effects. INHALATION TOXICOLOGY. Informa Healthcare USA, New York, NY, 1:2-13, (2015).
Impact/Purpose:
This is the first of a series of 8 papers examining susceptibility of various rodent cardiometabolic disease models to ozone induced health effects. This paper explains the origin of these models their clinical presentation of disease and the rationale for their use in examining susceptibility variations.
Description:
This is the first of a series of 8 papers examining susceptibility of various rodent cardiometabolic disease models to ozone induced health effects. Individuals with cardiovascular and metabolic diseases (CVD) are shown to be more susceptible to adverse health effects of pollutants. Rodent models of CVD are used for examining susceptibility variations. CVD models developed by selective inbreeding are shown to represent the etiology of human disease and metabolic dysfunction. The goal of this article was to review the origin and the pathobiological features of rat models of varying CVD with or without metabolic syndrome and healthy laboratory rat strains to allow better interpretation of the data regarding their susceptibility to air pollutant exposures.Age-matched healthy Sprague-Dawley (SD), Wistar (WIS) and Wistar Kyoto (WKY), and CVD-prone spontaneously hypertensive (SH), Fawn-Hooded hypertensive (FHH), SH stroke-prone (SHSP), SHHF/Moc; heart failure obese (SHHF) and insulin resistant JCR:LA-cp obese (JCR) rat models were considered for this study. The genetics and the underlying pathologies differ between these models. Normalized heart weights correlatedwith underlying cardiac disease while wide differences exist in the number of white blood cells and platelets within healthy strains and those with CVD. High plasma fibrinogen and low angiotensin converting enzyme activity in FHH might relate to kidney disease and associated hypertension. However, other obese strains with known kidney lesions do not exhibit decreases in ACE activity. The increased activated partial thromboplastin time only in SHSP correlates with their hemorrhagic stroke susceptibility. Increases plasma lipid peroxidation in JCR might reflect their susceptibility to acquire atherosderosis. These underlying pathologies involving CVD and metabolic dysfunction are critical in interpretation offindings related to susceptibility variations of air pollution health effects.
