Effects of diesel exhaust particles on blood pressure in rats.

The effects of diesel exhaust particles (DEP) on pulmonary functions and consequent diseases are well known, but there have been few reports concerning involvement of the cardiovascular system. In order to assess a direct action of DEP on cardiac tissue, the effects on blood pressure of intravenous administration of 12 or 120 mg/kg DEP to anesthetized rats were studied for a 15-min period. DEP (120 mg/kg) significantly lowered blood pressure for 25 s with no signs of arrhythmia or mortality, a phenomenon seen in guinea pigs. After 25 s blood pressure gradually returned to control levels and was maintained for 15 min. The 12-mg/kg DEP concentration did not markedly affect rat blood pressure. Pretreatment with atropine (24 mg/kg) blocked the DEP-induced fall in blood pressure, while pretreatment with propranolol (48 mg/kg) proved ineffective against DEP, suggesting involvement of the parasympathetic system. Data show that the rat is less sensitive to DEP-induced effects on blood pressure and may be a poor model to reflect cardiovascular changes.

Diesel exhaust (DE) affects the regulation of testicular function in male Fischer 344 rats.

To investigate the effects of diesel exhaust (DE) particles on the reproductive system, male Fischer 344 rats at 13 mo of age were exposed to clean air or DE at particle concentrations of 0.3, 1, or 3 mg/m3 for 8 mo. DE did not markedly affect testicular and body weights. However, DE at 0.3 mg/m3 significantly decreased prostate and coagulating gland weights, accompanied by a reduction in thymus and adrenal gland weight. In contrast, there was a significant rise in the weights of prostate, seminal vesicles, and coagulating glands in the 3 mg/m3 DE group. In rats exposed to 0.3 or 1 mg/m3 DE, serum luteinizing hormone (LH) and testosterone increased significantly, while a rise in testicular testosterone was noted with 3 mg/m3 DE. The concentrations of follicle-stimulating hormone (FSH) and inhibin as well as the sperm head counts were not markedly altered in any treatment group. Positive staining with inhibin-alpha subunit and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) were observed in Sertoli cells and Leydig cells, respectively. Immunolocalization of inhibin-alpha subunit and 3beta-HSD was not changed by exposure to DE. In conclusion, DE appears to exert greater effects on accessory glands than on testes in Fischer 344 rats, and the responsiveness of rats is less than that found in mice.