Sevoflurane

Sevoflurane depresses the activity of inspiratory premotor neurons in the caudal ventral medulla through a combination of reduced glutamatergic excitation and enhanced GABAergic inhibition. At 1 minimum alveolar concentration, sevoflurane depressed spontaneous neuronal activity by 30 percent. Overall glutamatergic excitation was decreased by 19.2 percent, while overall GABAAergic inhibition was enhanced by 11.9 percent. The postsynaptic responses to exogenous AMPA and NMDA were not significantly changed by sevoflurane, indicating that the reduction in glutamatergic excitation occurs through presynaptic mechanisms rather than postsynaptic receptor blockade. The study concluded that sevoflurane reduces neuronal activity primarily by decreasing presynaptic excitatory drive and increasing overall inhibitory input, without directly affecting postsynaptic AMPA or NMDA receptor function.

Fig. 1 The effect of Sevoflurane on overall neurotransmission. (Stucke A G.; et al. 2005)

Sevoflurane gel and microsphere formulations at different concentrations were developed to reduce occupational exposure when the drug is used topically for painful wound analgesia. Gel and microsphere formulations encapsulate sevoflurane to minimize volatilization into the workplace environment. Gel at 10 percent and microspheres at 30 percent produced modeled air levels below 2 ppm under demanding conditions. The microsphere formulation at equal concentration was found to be safer than gel from an occupational perspective. These new formulations represent a promising approach for developing topical sevoflurane products for wound pain treatment with improved occupational safety.

Fig. 2 Characterization of Sevoflurane gel and microsphere. (Gómez-Sánchez M T.; et al. 2025)