Department of Craniofacial Growth and Development Dentistry, Division of Orthodontics, Kanagawa Dental College, Yokosuka, Kanagawa Japan.
Am J Physiol Heart Circ Physiol. 2011 Oct;301(4):H1551-8. doi: 10.1152/ajpheart.01224.2010. Epub 2011 Aug 5.
Reducing stress is important in preventing sudden death in patients with cardiovascular disease, as stressful events may cause autonomic imbalance and trigger fatal arrhythmias. Since chewing has been shown to inhibit stress-induced neuronal responses in the hypothalamus, we hypothesized that chewing could ameliorate stress-induced autonomic imbalance and prevent arrhythmias. To test this hypothesis, we analyzed changes in radiotelemetered electrocardiograms in rats that were allowed to chew a wooden stick during a 1-h period of immobilization stress. Chewing significantly reduced the occurrence of ventricular premature beats (VPBs) and complex ventricular ectopy after immobilization and prevented stress-induced prolongation of the QT interval of VPBs throughout the 10-h experimental period. It also prevented prolongation of the QRS complex and fluctuations in the QT interval in normal sinus rhythm beats preceding VPBs during both immobilization and in the poststress period. Fast Fourier transform-based spectral analysis of heart-rate variability further showed that chewing significantly inhibited the stress-induced increase in the power ratio of low-to-high frequency activity (LF/HF: a marker of sympathetic activity) during immobilization and in addition was associated with blunting of the stress-induced increase in plasma noradrenaline observed at the termination of immobilization. Similar suppressive effects on the occurrence of VPBs and the LF/HF were observed in rats that were administered the β-adrenergic blocker propranolol before immobilization. These results indicate that chewing can ameliorate sympathetic hyperactivity during stress and prevent poststress arrhythmias and suggest that chewing may provide a nonpharmacological and cost-effective treatment option for patients with a high risk of stress-induced fatal arrhythmia.
减轻压力对于预防心血管疾病患者的猝死非常重要,因为应激事件可能导致自主神经失衡并引发致命性心律失常。由于咀嚼已被证明可以抑制下丘脑应激诱导的神经元反应,我们假设咀嚼可以改善应激引起的自主神经失衡并预防心律失常。为了验证这一假设,我们分析了在 1 小时固定应激期间允许大鼠咀嚼木棍时遥测心电图的变化。咀嚼显著减少了固定后室性早搏(VPB)和复杂室性异位的发生,并防止了应激引起的 VPB 的 QT 间期延长在整个 10 小时实验期间。它还防止了 QRS 复合物的延长和 VPB 之前正常窦性心律搏动中的 QT 间期波动在固定和应激后期间。基于快速傅里叶变换的心率变异性频谱分析进一步表明,咀嚼显著抑制了固定期间和固定结束时观察到的血浆去甲肾上腺素增加引起的交感神经活性增加(LF/HF:交感神经活动的标志物)。在固定之前给予β肾上腺素阻滞剂普萘洛尔的大鼠也观察到对 VPB 发生和 LF/HF 的类似抑制作用。这些结果表明,咀嚼可以改善应激期间的交感神经兴奋,并预防应激后心律失常,并表明咀嚼可能为应激诱导的致命性心律失常风险较高的患者提供一种非药物和具有成本效益的治疗选择。