Endotracheal Exposure of Particulate Matter Induces Arrhythmia via Oxidative Stress and Calcium Calmodulin Kinase II Activation

Hyelim Park, Eunmi Choi, Jin Bae Kim, Hui Nam Pak, Moon Hyoung Lee, Ki Chul Hwang, Boyoung Joung

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Backgrounds: Air pollution particulate matter (PM) could induce arrhythmia. We evaluated the arrhythmogenic mechanism of endotracheal exposure of PM. Methods: We compared the arrhythmic events in rats endotracheally exposed to diesel exhaust product (DEP) of 200 mg/L (DEP group, n=11), control (n=9) and DEP + N-acetylcysteine of 5 mmol/L (NAC group, n=3). Optical mapping was performed the day after in vivo experiment. Results: After endotracheal DEP exposure of 200 mg/L, PR (83 ±16 vs. 63 ±5 ms, p=0.02) and QT intervals (142 ±18, vs. 115±14 ms, p=0.02) were increased than baseline. However, compared with control, PR (73 ±6 ms, p=NS) and QT intervals (103 ±6 ms, p=NS) were not prolonged in NAC group. In DEP group, APD prolonged only at LV base (127±17, vs. 100±12 ms, p=0.002), increasing apicobasal APD (22±10, vs. 5± 11 ms, p=0.01) than control (n=8). Discordant alternans (94±12, vs. 128± 11 ms, p=0.001) were also easily induced at longer pacing cycle length in DEP group than in control. Ventricular arrhythmia was more frequently induced in DEP (67%) than control group (0%, p=0.01). Inhibition of calcium calmodulin kinase II (CaMKII) with KN 93 effectively protected cells from DEP-induced apotosis, whereas inactive KN 93 analogue, KN 92 had no protective effect. Conclusion: Endotracheal exposure of PM prolonged repolarization and induced arrhythmia via oxidative stress and CAMKII activation.

Original languageEnglish
Journaljournal of arrhythmia
Publication statusPublished - 2011 Jan 1


All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

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