Tracheal instillation of urban PM(2.5) suspension promotes acute cardiac polarization changes in rats.

The mechanisms by which PM(2.5) increases cardiovascular mortality are not fully identified. Autonomic alterations are the current main hypotheses. Our objective was to determine if PM(2.5) induces acute cardiac polarization alterations in healthy Wistar rats. PM(2.5) samples were collected on polycarbonate filters. Solutions containing 10, 20, and 50 microg PM(2.5) were administered by tracheal instillation. P wave duration decreased significantly at 20 microg (0.99 +/- 0.06, 0.95 +/- 0.06, and 0.96 +/- 0.07; P < 0.001), and 50 microg (0.98 +/- 0.06, 0.98 +/- 0.07, and 0.96 +/- 0.08; 60, 90 and 120 min, respectively) compared to blank filter solution (P < 0.001). PR interval duration decreased significantly at 20 microg (0.99 +/- 0.06, 0.98 +/- 0.07, and 0.97 +/- 0.08) and 50 microg (0.99 +/- 0.05, 0.97 +/- 0.0, and 0.95 +/- 0.05; 60, 90, and 120 min, respectively) compared to blank filter and 10 microg (P < 0.001). QRS interval duration decreased at 20 and 50 microg in relation to blank filter solution and 10 microg (P < 0.001). QT interval duration decreased significantly (P < 0.001) with time in animals receiving 20 microg (0.94 +/- 0.12, 0.88 +/- 0.14, and 0.88 +/- 0.11) and 50 microg (1.00 +/- 0.13; 0.97 +/- 0.11 and 0.98 +/- 0.16; 60, 90 and 120 min, respectively) compared to blank filter solution and 10 microg (P < 0.001). PM(2.5) induced reduced cardiac conduction time, within a short period, indicating that depolarization occurs more rapidly across ventricular tissue.