Desflurane and neural control of airway tone.

The study by Myers et al. in this edition of the Journal adds to our understanding of the role of desflurane in reactive airway disease. The authors compare the ability of sevoflurane with that of desflurane to alter respiratory mechanics following a cholinergic contraction in normal or sensitized rabbits whose lungs were ventilated through a tracheostomy. This study is an important addition to a growing body of literature which addresses an important clinical question: Does the choice of volatile anesthetic matter in patients with reactive airway disease, and more specifically, is desflurane a bad choice in patients with reactive airway disease? The airway is exposed to two primary irritants during general anesthesia with a volatile anesthetic, i.e., a foreign body (endotracheal tube or laryngeal mask airway device [LMAD]) acting as a mechanical irritant and a volatile anesthetic which can elicit a chemical irritation. C-fibres, including excitatory non-adrenergic non-cholinergic (eNANC) nerves, innervate the upper airway and are activated by transient receptor potential (TRP) channels to release tachykinins which can elicit smooth muscle contraction. Desflurane has been shown to activate TRP A1 receptors on C-fibres, inducing a tachykinin-mediated airway response. A secondary important neural reflex pathway which responds to airway irritation is the cholinergic pathway whereby parasympathetic nerve fibres travelling within the vagus nerve release acetylcholine which induces airway smooth muscle contraction. The current study was designed to evaluate the effect of desflurane on the neurotransmitter of this latter neural pathway, namely, acetylcholine. The authors demonstrate that desflurane is comparable with sevoflurane in its ability to attenuate bronchoconstriction induced by activation of muscarinic receptors on airway smooth muscle by intravenous methacholine. These results are consistent with previous studies which implicated TRP channels on C-fibres as the culprit of desflurane-induced bronchoconstriction observed in clinical studies. Although not a topic of the current study, desflurane activation of C-fibres would also account for the frequently observed clinical complication of cough. In isolated human bronchi, desflurane was equally potent as halothane and isoflurane at relaxing proximal but not distal bronchi. This finding is also consistent with the present study since neural innervation is thought to be primarily cholinergic in large central airways and eNANC in peripheral airways. In previous studies of isolated airways or tracheostomized and ventilated lungs of animals from multiple species, desflurane was shown to be at least as effective as other volatile anesthetics in directly relaxing airway smooth muscle. Taken together, these studies, which are performed in the absence of intact innervation, suggest that clinical difficulties with desflurane and the airway are not likely related to direct airway smooth muscle effects but are mediated by differential effects on irritant neural reflexes. The current study is an important addition to our mechanistic understanding of differential effects of volatile anesthetics on bronchoconstriction. This study demonstrates that sevoflurane and desflurane are similar in their abilities to prevent bronchoconstriction of cholinergic origin occurring in sensitized airways. It should be emphasized that desflurane was delivered to an intubated trachea (or isolated airway tissue) in this and previous C. W. Emala, MD (&) Department of Anesthesiology, Columbia University, 622 West 168th St., P&S Box 46, New York, NY 10032, USA e-mail: cwe5@columbia.edu