Abstract 16315: Opposing Effects of Dexmedetomidine and Fentanyl on Ciliary Beat Frequency in the Respiratory Epithelia
Introduction: Cilia beat frequency (CBF) in the ciliated airway epithelia determines the rate at which mucus is transported up the respiratory tract. Adequate transportation of mucus is required to provide a defense against respiratory infections. Previous studies have demonstrated when these cells are exposed to low temperature or certain anesthetics, their function can become impaired and CBF decreases. Both of these conditions are present when patients undergo surgery utilizing cardiopulmonary bypass and during their post-operative course in the ICU. Dexmedetomidine (dex) and fentanyl (fen) are two common anesthetics used in critically ill children with heart disease. We hypothesize dex and fen exposure in conjunction with hypothermia may suppress ciliary function in the respiratory epithelia.
Methods: C57BL/6J mouse tracheal epithelia were excised and placed ex vivo in L-15 medium at 15, 25, or 37°C with therapeutic concentration of dex (10nM), fen (10nM), dex+fen (10nM each) or with no drug added. Cilia dynamics were captured by videomicroscopy at 400 frames/sec using differential interference contrast (DIC) optics with a Phantom v4.2 camera.
Results: Exposure to dex caused reduction in CBF compared to control at 22-24°C (p=1.5E-5) and at 37°C (p=5.5E-7). In contrast, exposure to fen resulted in significant increases in CBF at 15°C (p=0.0032) and 22-24°C (p=0.0003). Interestingly, when dex and fen were combined, we observed significant recovery of CBF when compared to dex treatment alone at all three temperatures (p=0.019 at 15°C; p=4.1E-8 at 22-24°C; p=0.0002 at 37°C).
Conclusions: We observed dex and fen had opposing effects on ciliary motion in the airway. These findings suggest fen can be used to counteract the suppressive effects of dex on mucociliary clearance. The increase in CBF elicited by clinical doses of fen suggests possible therapeutic advantage in using fen in the perioperative and intensive care settings to improve post-surgical recovery.
- © 2011 by American Heart Association, Inc.