Heart rhythm · 2025
High subcutaneous nerve activity in noise-associated ventricular arrhythmias.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Chen Chao-Yi, Kuo Chia-Hao, Huang Tien-Chi, Yang Chao-Hui, Shih Jo-Yun, Lin Yi-Hsiung, Lin En-Ying, Lin Jia-Jhen, Hung Ming-Hsin, Huang Pin-Chieh, Chen Xin-Hui, Feng Yu-Chen, Zheng Ying-Xuan, Lin Min-Huei, Chen Guan-Lin, Lee Chien-Hung, Wu Chun-Chieh, Lee Hsiang-Chun, Wu Bin-Nan, Lin Shien-Fong, Lai Wen-Ter, Tsai Wei-Chung
Аннотация
BACKGROUND: Linked to autonomic nervous system (ANS) dysregulation, environmental noise is a contributing factor to cardiovascular disease and arrhythmias. Subcutaneous nerve activity (SCNA) and heart rate variability (HRV) are used to assess the ANS and arrhythmias in animal studies. The mechanisms underlying noise-induced arrhythmogenesis are unclear.
OBJECTIVE: This study aimed to determine the role of ANS modulation in noise-induced ventricular arrhythmias (VAs) by analyzing SCNA and HRV.
METHODS: C57BL/6 mice were grouped into noise-exposure or control groups and treated with either vehicle or 6-hydroxydopamine. The noise-exposure model was created using C57BL/6 mice exposed to broadband noise (20-20,000 Hz, 85 dB) for 28 days. Electrical signals were recorded using electrodes in the traditional lead I configuration for simultaneous electrocardiogram and SCNA measurements. Measurements were performed in 3 phases: baseline, cold pressor test, and recovery, each lasting 3 minutes. VA was defined as spontaneous premature ventricular contractions.
RESULTS: Noise exposure induced a state of sympathetic hyperactivity, evidenced by significantly higher SCNA (P ≤ .030) and lower HRV parameters (P ≤ .034) than controls. This sympathetic mediation was confirmed by chemical sympathectomy, 6-hydroxydopamine, which blunted the SCNA increase (P ≤ .012). Functionally, this autonomic dysregulation led to increased arrhythmogenesis; during a cold pressor test, the noise + vehicle group developed significantly more premature ventricular contractions (P = .013), 81% of which were directly preceded by SCNA bursts.
CONCLUSION: Noise exposure increases SCNA and induces VA via sympathetic activation, an effect that was inhibited by 6-hydroxydopamine. This confirms autonomic dysregulation as the central mechanism and validates SCNA as a feasible assessment tool in mice.
OBJECTIVE: This study aimed to determine the role of ANS modulation in noise-induced ventricular arrhythmias (VAs) by analyzing SCNA and HRV.
METHODS: C57BL/6 mice were grouped into noise-exposure or control groups and treated with either vehicle or 6-hydroxydopamine. The noise-exposure model was created using C57BL/6 mice exposed to broadband noise (20-20,000 Hz, 85 dB) for 28 days. Electrical signals were recorded using electrodes in the traditional lead I configuration for simultaneous electrocardiogram and SCNA measurements. Measurements were performed in 3 phases: baseline, cold pressor test, and recovery, each lasting 3 minutes. VA was defined as spontaneous premature ventricular contractions.
RESULTS: Noise exposure induced a state of sympathetic hyperactivity, evidenced by significantly higher SCNA (P ≤ .030) and lower HRV parameters (P ≤ .034) than controls. This sympathetic mediation was confirmed by chemical sympathectomy, 6-hydroxydopamine, which blunted the SCNA increase (P ≤ .012). Functionally, this autonomic dysregulation led to increased arrhythmogenesis; during a cold pressor test, the noise + vehicle group developed significantly more premature ventricular contractions (P = .013), 81% of which were directly preceded by SCNA bursts.
CONCLUSION: Noise exposure increases SCNA and induces VA via sympathetic activation, an effect that was inhibited by 6-hydroxydopamine. This confirms autonomic dysregulation as the central mechanism and validates SCNA as a feasible assessment tool in mice.