title: Chewing reduces sympathetic nervous response to stress and prevents poststress arrhythmias in rats.
abstract: 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.
authors.affiliation: Department of Craniofacial Growth and Development Dentistry, Division of Orthodontics, Kanagawa Dental College, Yokosuka, Kanagawa Japan.
authors.forename: So
authors.initials: S
authors.lastname: Koizumi
authors.forename: Susumu
authors.initials: S
authors.lastname: Minamisawa
authors.forename: Kenichi
authors.initials: K
authors.lastname: Sasaguri
authors.forename: Minoru
authors.initials: M
authors.lastname: Onozuka
authors.forename: Sadao
authors.initials: S
authors.lastname: Sato
authors.forename: Yumie
authors.initials: Y
authors.lastname: Ono
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000517:prevention & control*; D002395:Catecholamines / Q000097:blood; D004562:Electrocardiography / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D008297:Male; D008409:Mastication / Q000502:physiology*; D010275:Parasympathetic Nervous System / Q000502:physiology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical; D013315:Stress, Psychological / Q000150:complications / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology*; D013686:Telemetry; D018879:Ventricular Premature Complexes / Q000517:prevention & control
chemical_list: D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D011433:Propranolol