School of Medicine and Health Sciences Poster Presentations
Impaired Autonomic Regulation in Posttraumatic Stress Disorder
Poster Number
22
Document Type
Poster
Publication Date
3-2016
Abstract
Post-traumatic stress disorder (PTSD) is associated with a significantly increased risk of cardiovascular disease (CVD) and accumulating clinical evidence suggests that autonomic dysregulation due to sympathetic overactivity and/or parasympathetic insufficiency may contribute to progression of CVD in PTSD. Therefore, utilizing a translational approach, we sought to examine autonomic function in both a clinical PTSD population as well as in an animal model of PTSD. In experimental studies, mice were instrumented with radiotelemetry probes to evaluate autonomic indices following Pavlovian fear conditioning. Fear conditioning involves the pairing of a conditioned stimulus (e.g. tone) paired with an aversive uconditioned stimulus (e.g. foot shock) that evokes a conditioned response (e.g. freezing). Twenty-four hours following fear conditioning, spectral analysis of heart rate was performed and the low-to high-frequency ratio (LF:HF) was used as an index of sympathovagal balance. Fear conditioned animals displayed a significant increase in the LF:HF ratio relative to baseline (1.21 ± 0.46;; pfall in blood pressure compared to control (Δ Systolic -71.7± 1.9 vs -39.8 ± 5.8 mmHg;; p24-hour ambulatory BP measurements have been collected at rest, during, and following mental stress. In an effort to translate our pre-clinical results, these data will be analyzed for spectral analysis of heart rate variability, BP variability, and 24-hour ambulatory BP patterns.
Support or Funding Information
NIH R00 HL107675-03 American Heart Association - 15CSA24340001
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
Open Access
1
Impaired Autonomic Regulation in Posttraumatic Stress Disorder
Post-traumatic stress disorder (PTSD) is associated with a significantly increased risk of cardiovascular disease (CVD) and accumulating clinical evidence suggests that autonomic dysregulation due to sympathetic overactivity and/or parasympathetic insufficiency may contribute to progression of CVD in PTSD. Therefore, utilizing a translational approach, we sought to examine autonomic function in both a clinical PTSD population as well as in an animal model of PTSD. In experimental studies, mice were instrumented with radiotelemetry probes to evaluate autonomic indices following Pavlovian fear conditioning. Fear conditioning involves the pairing of a conditioned stimulus (e.g. tone) paired with an aversive uconditioned stimulus (e.g. foot shock) that evokes a conditioned response (e.g. freezing). Twenty-four hours following fear conditioning, spectral analysis of heart rate was performed and the low-to high-frequency ratio (LF:HF) was used as an index of sympathovagal balance. Fear conditioned animals displayed a significant increase in the LF:HF ratio relative to baseline (1.21 ± 0.46;; pfall in blood pressure compared to control (Δ Systolic -71.7± 1.9 vs -39.8 ± 5.8 mmHg;; p24-hour ambulatory BP measurements have been collected at rest, during, and following mental stress. In an effort to translate our pre-clinical results, these data will be analyzed for spectral analysis of heart rate variability, BP variability, and 24-hour ambulatory BP patterns.
Support or Funding Information
NIH R00 HL107675-03 American Heart Association - 15CSA24340001
Comments
Presented at: GW Research Days 2016