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Cardiorespiratory Coupling is Dependent on a Conditionally Expressed Inspiratory Antecedent in the In Situ Rodent Preparation
Author(s) -
Baekey David M
Publication year - 2016
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.30.1_supplement.988.9
Subject(s) - bursting , respiratory system , perfusion , phrenic nerve , medulla oblongata , rostral ventrolateral medulla , cardiorespiratory fitness , population , heart rate , anesthesia , chemistry , medicine , neuroscience , blood pressure , cardiology , anatomy , biology , central nervous system , environmental health
The in situ rodent model was previously used to describe respiratory modulation of cardiovascular activities expressed in heart rate (RSA), sympathetic nerves (SNA), and vascular pressure. While this previous study implicated both medullary and pontine involvement, the neural substrate for this coordination remains undefined. Our hypothesized model assumes some direct connectivity within the medulla, wherein the respiratory central pattern generating (rCPG) nuclei influence more caudal premotor respiratory populations (VRG) and adjacent autonomic nuclei (RVLM/CVLM), but recent observations challenge the straightforwardness of this proposed network. A retrospective analysis of 37 preparations in which the phrenic nerve was recorded prior to the first reanimated breath revealed features suggesting involvement of a unique inspiratory neural population. To observe this coupling, juvenile rats are anaesthetized, subdiaphragmatically bisected, decerebrated, and submerged in ice cold artificial cerebrospinal fluid (aCSF) during surgical exposure of neural recording sites. Aortic cannulation and perfusion with aCSF warms the preparations and provides dissolved O 2 and CO 2 (95/5) while electrodes are placed to monitor respiratory and autonomic nerves. A gradual increase in perfusion flow results in respiratory efforts as noted by both visible contraction of the chest musculature prior to application of paralytic and bursting activity of respiratory efferents thereafter. Phrenic nerve activity (PNA) has a relatively consistent expression at 12–15 breaths per minute with no initial coordination of heart rate, modulation of SNA, or oscillations of perfusion pressure. As phrenic bursting continues, one of two patterns occurs: 1) a sudden transition to ramp patterned PNA with reduced Ti and increased Te (N=30), or 2) high amplitude, short duration phrenic bursts are interspersed amongst the stable baseline rhythm, eventually entraining and merging with the baseline pattern to form the ramping phrenic with reduced Ti and increased Te (N=7). The significance of both pattern changes is that they occur simultaneously with expression of RSA and respiratory modulation of vascular pressure. In the interspersed expression, cardiorespiratory coupling was limited to the short duration, high amplitude bursts. In summary, this suggests that cardiorespiratory coupling requires activation of a conditionally expressed neural population that is active during late inspiration. Given that cardio‐respiratory coupling is reduced with aging and decreased RSA is proposed as a predictor of mortality, identification and modulation of this “missing link” might provide a powerful therapeutic target in prevention of cardiovascular disease. Support or Funding Information This research was supported by a UF CVM Faculty Award.