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Published on: April 7, 2021
Dynamics of ventilatory pattern variability and Cardioventilatory Coupling during systemic inflammation in rats
Cara K Campanaro1, David E Nethery1, Fei Guo2
1Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Case Western Reserve University, Cleveland, OH, United States.
Endotoxemia, induced by lipopolysaccharide (LPS), altered ventilatory pattern variability (VPV) and cardioventilatory coupling (CVC) in rats. The Nonlinear Complexity Index (NLCI) for VPV increased, while CVC decreased, indicating sensitivity to sepsis-induced neuroinflammation.
Area of Science:
- Physiology
- Neuroscience
- Biomedical Engineering
Background:
- Physiologic signals offer insights into health status.
- Ventilatory Pattern Variability (VPV) and Cardioventilatory Coupling (CVC) are key biometric measures.
- Endotoxemia can induce neuroinflammation, potentially affecting these measures.
Purpose of the Study:
- To investigate the sensitivity of VPV and CVC to endotoxemia.
- To assess the impact of lipopolysaccharide (LPS) on neuroinflammation and respiratory/cardiac biometrics.
- To evaluate the Nonlinear Complexity Index (NLCI) as a measure of VPV changes.
Main Methods:
- Rats were implanted with blood pressure (BP) transducers.
- Ventilatory waveforms and BP were recorded using whole-body plethysmography.
- LPS or saline was administered intraperitoneally for 3 days, with subsequent analysis of VPV, CVC, and heart rate variability (HRV).
Main Results:
- Heart rate (HR) and respiratory frequency (fR) increased, while CVC decreased in LPS-treated rats.
- NLCI, a measure of VPV, increased, indicating greater waveform predictability.
- BP and HRV spectral components (LF, HF) showed no significant changes; lung injury and IL-1β in respiratory nuclei were confirmed.
Conclusions:
- NLCI effectively reflects health changes induced by LPS-induced endotoxemia.
- Changes in VPV and CVC are sensitive indicators of systemic inflammation and neuroinflammation.
- NLCI may represent the influence of inflammatory cytokines on the respiratory control network.
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