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

Hyelim Park, Eunmi Choi, Jin Bae Kim, huinam pak, Moon Hyoung Lee, Ki Chul Hwang, Boyoung Joung

Research output: Contribution to journalArticle

Abstract

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
Volume27
DOIs
Publication statusPublished - 2011 Jan 1

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Vehicle Emissions
Calcium-Calmodulin-Dependent Protein Kinases
Particulate Matter
Cardiac Arrhythmias
Oxidative Stress
Calcium
pamidronate
Control Groups
Air Pollution
Acetylcysteine

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

@article{c0ee3012a0274b68ae4f0f2185ff9241,
title = "Endotracheal Exposure of Particulate Matter Induces Arrhythmia via Oxidative Stress and Calcium Calmodulin Kinase II Activation",
abstract = "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.",
author = "Hyelim Park and Eunmi Choi and Kim, {Jin Bae} and huinam pak and Lee, {Moon Hyoung} and Hwang, {Ki Chul} and Boyoung Joung",
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language = "English",
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journal = "Journal of Arrhythmia",
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Endotracheal Exposure of Particulate Matter Induces Arrhythmia via Oxidative Stress and Calcium Calmodulin Kinase II Activation. / Park, Hyelim; Choi, Eunmi; Kim, Jin Bae; pak, huinam; Lee, Moon Hyoung; Hwang, Ki Chul; Joung, Boyoung.

In: journal of arrhythmia, Vol. 27, 01.01.2011.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Endotracheal Exposure of Particulate Matter Induces Arrhythmia via Oxidative Stress and Calcium Calmodulin Kinase II Activation

AU - Park, Hyelim

AU - Choi, Eunmi

AU - Kim, Jin Bae

AU - pak, huinam

AU - Lee, Moon Hyoung

AU - Hwang, Ki Chul

AU - Joung, Boyoung

PY - 2011/1/1

Y1 - 2011/1/1

N2 - 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.

AB - 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.

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