Answer:

The volatile anesthetics relax airway smooth muscle primarily by directly reducing smooth muscle contractility and indirectly by inhibiting the reflex neural pathways. Direct effects of the volatile anesthetics partially depend on intact bronchial epithelium, suggesting that epithelial damage or inflammation secondary to asthma or a respiratory infection may lessen their bronchodilating effect.

The mechanisms responsible for the direct relaxation effects involve decreases in intracellular calcium, an important regulator of smooth muscle reactivity. Several intracellular mediators responsible for mobilization of calcium ions are potential sites for the action of volatile anesthetics, but the predominant mechanism appears to be inhibition of cell membrane-associated voltage-dependent calcium channels, an action that decreases entry of calcium ions into the cytosol. Volatile anesthetic-induced increases in cyclic 3′,5′ adenosine monophosphate (cAMP) cause decreases in free intracellular calcium by stimulating efflux of calcium and increasing uptake of calcium into the sarcoplasmic reticulum. This action contributes to airway smooth muscle relaxation. In addition, volatile anesthetics reduce calcium sensitivity as a result of inhibition of protein kinase C activity and inhibition of G protein function.

• Barash PG, Cullen BF, Stoelting RK, et al, eds. Clinical Anesthesia. 8th ed. Philadelphia, PA: Wolters Kluwer; 2017:478-479.
• Gropper MA, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 9th ed. Philadelphia, PA: Elsevier; 2020:543-546.