Recent data suggest that ultrafine pollutant particles (diameter <0.1 μm) may pass from the lung into the systemic circulation. However, the systemic and cardiorespiratory effects of translocated particles are not well known. In this study, we determined the direct acute (24 h) effect of the systemic administration of 0.01 mg/kg and 0.02 mg/kg diesel exhaust particles (DEP) on systolic blood pressure, heart rate, and both systemic and pulmonary inflammation in spontaneously hypertensive rats (SHR). Compared to the blood pressure in control group, rats exposed to DEP exhibited a dose-dependent increase in systolic blood pressure, at 0.01 mg/kg (P < 0.05) and 0.02 mg/kg (P < 0.01). Likewise, the heart rate was also dose-dependently increased at 0.01 mg/kg (P:NS) and 0.02 mg/kg (P < 0.01) compared to control SHR. DEP exposure (0.02 mg/kg) significantly elevated the number of leukocytes in blood (P < 0.05), interleukin-6 (IL-6, P < 0.005), tumor necrosis factor alpha (P < 0.05) and leukotriene B4 (LTB4, P < 0.005) concentrations in plasma. Moreover, in SHR given 0.02 mg/kg, the number of platelet was significantly reduced (P < 0.05), whereas the tail bleeding time was prolonged (P < 0.05). Pulmonary inflammations were confirmed by the presence of a significant increase in the number of macrophages (0.02 mg/kg) and neutrophils (0.01 and 0.02 mg/kg) and protein contents (0.02 mg/kg) in bronchoalveolar lavage (BAL) compared to saline-treated SHR. Also, IL-6 (0.01 mg/kg; P < 0.05 and 0.02 mg/kg; P < 0.01), LTB4 (0.02 mg/kg; P < 0.05) concentrations in BAL and the superoxide dismutase activity (0.02 mg/kg; P = 0.01) were significantly elevated compared to control group. We conclude that, in SHR, the presence of DEP in the systemic circulation leads not only to cardiac and systemic changes, but also triggers pulmonary inflammatory reaction involving IL-6, LTB4 and oxidative stress.
- Diesel exhaust particles
- Lung inflammation
- Spontaneously hypertensive rats
- Systemic inflammation
ASJC Scopus subject areas