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Particulate Air Pollution Effects on Autonomic Dysfunction and the Arrhythmogenesis in rat model with ischemic injury
관동대학교 의과대학 내과학교실 심장내과¹ , 연세대학교 의과대학 내과학 교실 심장내과 ². 심혈관 연구소 ³
김진배¹, 이창연³ , 송병욱³ , 황혜진² , 정보영² , 이문형² , 김성순²
Introduction: It has been shown that ambient air pollution leads to increased cardiovascular mortality, and studies found associations between ambient air pollution and hospital admissions for various cardiovascular diseases. In this study, the effects of air pollutants on cardiac arrhythmia and heart rate variability (HRV) were evaluated and the mechanism of arrhythmogenesis was elucidated. Materials and methods: we will use the ambient PM exposure collected using portable mini volume sampler during morning (AM 7:00 ~ AM 10). This particle matters was instillated via trachea to isoproterenol induced myocardiac injury rat medel. Twenty-four hours after exposure, the animals are lightly anesthetized and 3 ml of blood will be collected by cardiac puncture. Echocardiography was performed for evaluation of cardiac function. Ex-vivo ventricular arrhythmia induction was performed by electrical stimulator. Optical mapping was performed. Telemetry monitoring was recorded during all procedure and HRV (heart rate variability) was acquired. Results: There were no significant difference between control and PM instillation group in Ventricular tachyarrhythmia(VT/VF) occurrence: 3.1±1.2 times in control group vs 2.5±0.6 times in PM group, p=0.3; There were significant difference in HRV parameters (mean NN, SDNN, SDANN, RMSSD, p=0.03). In optical mapping, there were significant difference of action potential duration at 70%(APD70) between control and PM group at normal(37.1±32.2ms vs 31.0±34.3ms), borderzone (59.7±51.8ms vs 80.8±48.7ms) and infarction area(89.4±47.4ms vs 122.8±24.0ms) respectively(p=0.86 , p=0.04 and p=0.03). there was no significant difference in infarcted myocardium(H-E stain; control vs PM, 29.1% vs 29.5%, p=0.85) Conclusion: ambient PM exposure affect the autonomic function and arrhythmogenesis in infracted heart without change of heart function or infarcted myocardiac size.


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