Contrasting open-loop dynamic characteristics of sympathetic and vagal systems during baroreflex-mediated heart rate control in rats

Abstract

Although heart rate (HR) is governed by the sympathetic and parasympathetic nervous systems, a head-to-head comparison of the open-loop dynamic characteristics of the total arc from a baroreceptor pressure input to the HR response has yet to be performed. We estimated the transfer function from carotid sinus pressure input to the HR response ( HCSP→HR) before and after bilateral vagotomy ( n = 7) as well as before and after the administration of a β-blocker propranolol ( n = 8) in anesthetized male Wistar-Kyoto rats. The carotid sinus pressure was perturbed according to a Gaussian white noise signal so that the input power spectra were relatively flat between 0.01 and 1 Hz. The gain plot of HCSP→HR was V-shaped. Vagotomy reduced the dynamic gain at 1 Hz (0.0598 ± 0.0065 to 0.0025 ± 0.0004 beats·min−1·mmHg−1, P < 0.001) but not at 0.01 or 0.1 Hz. β-Blockade reduced the dynamic gain at 0.01 Hz (0.247 ± 0.069 to 0.077 ± 0.017 beats·min−1·mmHg−1, P = 0.020) but not at 0.1 or 1 Hz. We also estimated the efferent limb transfer function from electrical vagal efferent stimulation to the HR response ( HVN→HR) under β-blockade conditions. We associated the model parameters of HVN→HR with the mean HR and the standard deviation of HR so that HVN→HR could be estimated based only on the HR data. We finally estimated the neural arc transfer function from a pressure input to efferent vagal nerve activity by dividing HCSP→HR by HVN→HR. The mathematically determined vagal neural arc showed derivative characteristics with its phase near zero radians at the lowest frequency.

Effects of Spinal Cord Injury Site on Cardiac Autonomic Regulation: Insight from Analysis of Cardiovascular Beat by Beat Variability during Sleep and Orthostatic Challenge

“…In this study, we have reported preliminary observations on a small group of Spinal Cord-Injured patients with either proximal (cervical) or distal (thoracic) lesions. This particular clinical experimental model, in spite of the small number of subjects [41], showed that SCI impaired sympathetic positive feedback reflexes [15], while sparing selectively negative feedback reflexes that depend on an intact vagal innervation [43]. In particular SCI patients were characterized by reduced responses to spontaneous and physiologically induced sympathetic activation (as produced by REM sleep [26] and tilt, respectively [23,27] when considering RRLFnu and RRHFnu, markers of sympatho-vagal balance.…”

“…The same occurred considering the changes induced by tilt or by REM sleep, as expected considering that pathways followed by parasympathetic (vagal) fibers, that interconnect the medulla oblongata directly with the periphery, are not affected by SCI. Many studies in the literature have shown that time domain indices and indices of baroreflex gain reflect mainly parasympathetic control [30,43,46,47].…”

“…Here, we have reported data from a small observational study about the feasibility of assessing the functional derangement accompanying proximal or distal SCI utilizing loop models [43] and a combination of clinical/statistical tools [25]. Monovariate or multivariate analysis from cardiovascular variability [10] provided data that were descriptors of the functional impairment, according to the site of the injury [49].…”