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Quantitative evaluation of pulmonary stretch receptor activity during high-frequency ventilation
S L Thompson-Gorman1, R S Fitzgerald, W Mitzner
1Department of Environmental Health Sciences (Division of Physiology), School of Hygiene and Public Health, Johns Hopkins University, Baltimore, Maryland 21205.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|March 1, 1992
Summary
Pulmonary stretch receptors (PSRs) show increased firing with higher airway pressure and tidal volume. High-frequency ventilation (HFV) did not alter the overall neural output of PSRs compared to conventional mechanical ventilation (CMV).
Area of Science:
- Respiratory Physiology
- Neuroscience
- Pulmonary Medicine
Background:
- Pulmonary stretch receptors (PSRs) are mechanoreceptors in the lungs that signal lung volume and mechanical forces.
- Previous studies indicated that specific mechanical ventilation conditions can induce apnea in cats.
- Understanding PSR neural output is crucial for assessing their role in ventilation-induced apnea.
Purpose of the Study:
- To determine the neural output of pulmonary stretch receptors (PSRs).
- To investigate PSR responses under conditions previously shown to cause apnea.
- To assess the specific contribution of PSRs to apnea during mechanical ventilation.
Main Methods:
- Recorded activity of individual PSRs in anesthetized cats.
- Exposed PSRs to high-frequency ventilation (HFV) with varying airway pressure (Paw), tidal volume, and inspired CO2.
- Compared PSR activity during HFV to conventional mechanical ventilation (CMV).
Main Results:
- PSRs exhibited continuous activity correlated with pump stroke.
- PSR firing rate increased significantly with higher mean Paw (6 cmH2O vs. 2 cmH2O) and larger tidal volumes.
- At 2 cmH2O Paw, HFV did not alter the number of PSR impulses per second compared to CMV.
Conclusions:
- The absolute amount of inhibitory afferent signal from PSRs during HFV was not different from CMV.
- The contribution of PSRs to HFV-induced apnea likely stems from altered signal patterns or central processing.
- Findings suggest that changes in the timing or interpretation of PSR signals, not signal quantity, mediate apnea.