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Clinical and pathological manifestations of cardiovascular disease in rat models: the influence of acute ozone exposure
Citation:
Ramot, Y., U. Kodavanti, G. Kissling, A. Ledbetter, AND A. Nyska. Clinical and pathological manifestations of cardiovascular disease in rat models: the influence of acute ozone exposure. INHALATION TOXICOLOGY. Informa Healthcare USA, New York, NY, 1:26-38, (2015).
Impact/Purpose:
This paper shows that rat models of cardiovascular diseases have differential degrees of underlying pathologies at a young age. Sever kidney lesions were noted in some but not all models suggesting that each cardiovascular disease might originate from different causes and express complications in multiple organs. This information is critical in understand how air pollution might exacerbate the disease in these models. Ozone induced lung pathologies varied in these models.
Description:
This paper shows that rat models of cardiovascular diseases have differential degrees of underlying pathologies at a young age. Rodent models of cardiovascular diseases (CVD) and metabolic disorders are used for examining susceptibility variations to environmental exposures. However, cross-model organ pathobgies and clinical manifestations are often not compared. We hypothesized that genetic CVD rat models will exhibit baseline pathologies and will thus express varied lung response to acute ozone exposure. Male 12-14-week-old healthy Wistar Kyoto (WKY), Wistar (WIS), and Sprague Dawley (SD) rats and CVD-compromised spontaneously hypertensive(SH), fawn-hooded hypertensive (FHH), stroke-prone SH (SHSP), obese SH heart-failure (SHHF), obese diabetic JCR (JCR) rats were exposed to 0.0, 0.25, 0.5, or 1.0 ppmozone for 4 h and clinical biomarkers, and lung, heart and kdney pathologies were compared immediately following (0-h) or 20-h later. Strain differences were observed between air-exposed CVD-prone and WKY rats in clinical biomarkers and in kidney and heart pathology. Serum cholesterol was higher in air-exposed obese SHHF and JCR compared to other air-exposed strains. Ozone did not produce lesions in the heart or kidney. CVD-prone and SD rats derronstrated glomerulopathy and kidney inflammation (WKY = WIS = SH < SD = SHSP < SHHF < JCR = FHH) regardless of ozone. Cardiac myofiber degeneration was evident in SH, SHHF, and JCR, while only JCR tends to have inflammation in coronaries. Lung pathology in air-exposed rats was minimal in all strains except JCR. Ozone induced variable alveolar histiocytosis and bronchiolar inflammation; JCR and SHHF were less affected. This study provides a comparative account of the clinical manifestations of disease and early-life organ pathologies in several rat models of CVD and their differential susceptibility to lung injury from air pollutant exposure.
