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Effects of weight‐reducing chronic vagal nerve stimulation on cardiovascular, autonomic, and respiratory functions (1126.12)
Author(s) -
Stauss Harald,
Morgan Donald,
Rahmouni Kamal
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1126.12
Subject(s) - medicine , bradycardia , blood pressure , anesthesia , heart rate , stimulation , autonomic nervous system , vagal tone , heart rate variability , tachycardia , ventilation (architecture) , respiratory system , cardiology , mechanical engineering , engineering
We assessed potential cardiovascular, autonomic, and respiratory adverse effects of chronic vagal nerve stimulation (VNS). In normotensive rats on standard diet, cervical vagal nerve stimulators were turned on 24 h after surgical implantation or remained off (sham) for the remainder of the study (up to 29 days). After one week of VNS, body weight was reduced by 27% while sham‐treated rats had restored pre‐surgical weight. Chronic VNS caused bradycardia that turned into tachycardia when the stimulators were temporarily turned off. VNS also resulted in hypertension that persisted when the stimulators were turned off. Compared to sham rats, high frequency heart rate variability (parasympathetic cardiac modulation) was markedly increased and low frequency systolic blood pressure variability (sympathetic modulation of vascular tone) was reduced when the stimulators were on, but not when they were off. In rats with chronic VNS a gasping‐like breathing pattern was occasionally noted. Furthermore, respiratory effort assessed by high frequency (respiration‐linked) spectral power of systolic blood pressure, was enhanced in rats with chronic VNS when the stimulators were temporarily turned off. In conclusion, weight‐reducing chronic VNS potentially causes reversible bradycardia, sustained hypertension that cannot be explained by elevated sympathetic modulation of vascular tone, and respiratory distress. Grant Funding Source : Supported by NIH (HL084207 KR), ADA (1‐11‐BS‐127, KR), UI Fraternal Order of Eagles Diabetes Center