Neural Mechanism Facilitating PM2.5-Related Cardiac Arrhythmias Through Cardiovascular Autonomic and Calcium Dysregulation in a Rat Model

Abstract

Abstract Background Particulate matter<2.5μm (PM2.5) exposure is associated with increased arrhythmia events and cardiovascular mortality, but the detailed mechanism remained elusive. In the current study, we aimed to investigate autonomic alterations in rats after acute exposure to PM2.5. Methods Twelve male WKY rats were randomized to control and PM2.5 groups. All were treated with 2 exposures of oropharyngeal aerosol inhalations (1μg PM2.5 per gram of body weight in 100uL normal saline for PM2.5 group) separately by 7 days. Polysomnography and electrocardiography were performed. Physiologic monitors were used to define active waking (AW), quiet, and paradoxical sleep (QS, PS). Autonomic regulations were measured by heart rate variability (HRV). The protein expression of ventricular tissue of the 2 groups were compared at the end of the experiment. Results In sleep pattern analysis, QS interruption of the PM2.5 group was significantly higher than the control group (0.52± 0.04events/min, 0.33± 0.04events/min, p=0.024). In HRV analysis, the LF/HF was significantly higher for the PM2.5 group than the control group (0.66± 0.13, 1.16± 0.05, p=0.009), largely driven by LF/HF increase during the QS phase. Ionic channel protein expression from Western blots showed that the PM2.5 group had significantly lower L-type calcium channel, and higher SERCA2 and rectifier potassium channel expressions than the control group, respectively. Conclusion Our results showed that PM2.5 exposure leads to interruption of QS, sympathetic activation, and recruitment of compensatory calcium handling proteins. The autonomic and calcium dysregulations developed after PM 2.5 exposure may explain the risk of sleep disturbance and sleep-related arrhythmia.