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Influence of lung inflation reflex on vascular capacitance in the systemic circulation
1Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, 53226.
The American Journal of Physiology
|November 1, 1989
Summary
Sustained lung inflation in dogs triggers a reflex that increases systemic vascular capacitance and decreases systemic vascular resistance and sympathetic nerve activity. This lung inflation reflex is primarily mediated by vagal afferent nerve fibers.
Area of Science:
- Physiology
- Cardiovascular System
- Respiratory System
Background:
- Understanding the cardiovascular reflexes initiated by lung inflation is crucial for managing respiratory and cardiac conditions.
- Previous research has explored the effects of lung mechanics on cardiovascular parameters, but the specific neural pathways involved require further elucidation.
Purpose of the Study:
- To investigate the impact of sustained lung inflation on systemic vascular capacitance (SVC), systemic vascular resistance (SVR), and cardiac sympathetic efferent nerve activity (SENA).
- To determine the role of vagal afferent nerve fibers in mediating the observed cardiovascular responses to lung inflation.
Main Methods:
- Anesthetized dogs were subjected to total cardiopulmonary bypass.
- Sustained lung inflation was induced by inflating lungs to tracheal pressures of 10, 15, and 20 mmHg.
- Measurements of SVC, SVR, and SENA were recorded, with and without bilateral vagotomy, at a low carotid sinus pressure (CSP) of 41 mmHg.
Main Results:
- Lung inflation significantly increased SVC and decreased SVR in a pressure-dependent manner.
- Cardiac sympathetic efferent nerve activity (SENA) decreased concurrently with lung inflation.
- Bilateral vagotomy substantially attenuated the changes in SVR, SVC, and SENA, indicating a primary role for vagal afferents.
Conclusions:
- Lung inflation elicits a reflex that increases systemic vascular capacitance and reduces systemic vascular resistance and sympathetic nerve activity.
- The lung inflation reflex is predominantly mediated by vagal afferent nerve fibers, with a minor contribution from other afferent pathways.