Related Experiment Videos
Site(s) mediating sympathetic activation with desflurane
1Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, USA.
Anesthesiology
|October 1, 1996
Summary
Desflurane activates sympathetic responses via upper airway and lung receptors, independent of systemic effects. Lidocaine did not attenuate these desflurane-induced neurocirculatory changes.
Area of Science:
- Anesthesiology
- Neurophysiology
Background:
- Desflurane's neurocirculatory activation mechanism requires precise identification of afferent pathways.
- Understanding these pathways is crucial for safe anesthetic administration.
Purpose of the Study:
- To delineate the specific afferent sites responsible for desflurane-induced neurocirculatory activation.
- To investigate the role of upper airway and pulmonary receptors in this response.
Main Methods:
- Three studies in healthy volunteers (aged 19-28) monitored cardiovascular and sympathetic responses.
- Desflurane was selectively delivered to upper/lower airways or lungs using double-lumen tubes.
- Lidocaine or placebo was administered to assess its effect on desflurane's neurocirculatory activation.
Main Results:
- Desflurane directed to the upper airway caused significant increases in heart rate, blood pressure, and sympathetic activity.
- Delivery to the lungs induced even greater neurocirculatory responses, independent of systemic desflurane levels.
- Lidocaine administration did not attenuate the observed desflurane-induced neurocirculatory activation.
Conclusions:
- Both upper airway (laryngeal) and pulmonary sites initiate sympathetic activation during desflurane administration.
- These responses are partly independent of systemic anesthetic concentrations.
- The findings suggest direct airway mucosal irritation and distinct pulmonary reflexes contribute to desflurane's effects.