2009

Main conclusions:

1. Sevoflurane slowly depolarizes the mitochondrial membrane in isolated CNS presynaptic terminals, and this effect is not dependent on Ca²⁺-influx to the cytosol. Opening of mitoK_ATP is only partly responsible for this depolarizing effect of sevoflurane.

2. Isoflurane and sevoflurane depolarize presynaptic mitochondria through inhibition of the electron transport chain. Isoflurane seems to inhibit mitochondrial function more pronounced than sevoflurane. Both agents inhibit the respiratory chain sufficiently to cause ATP synthase reversal.

3. Isoflurane depolarizes the mitochondrial membrane potential (Δψ_m) of neural mitochondria in an age dependent manner by inhibition of the respiratory chain. The effect is more pronounced in the adolescent and adult than in neonatal rats.

4. Sevoflurane and propofol at equipotent doses depolarize the mitochondria in rat and human nerve terminals to the same extent. The depolarizing effect of propofol on the Δψ_{m was more rapid in onset than that of sevoflurane. Whereas sevoflurane inhibits the respiratory chain sufficiently to cause ATP synthase reversal, the depolarizing effect of propofol seems to be related to inhibition of the respiratory chain from complex I-V.}

Moe MC, Bains R, Vinje ML, Larsen GA, Kampenhaug EB, Berg-Johnsen J (2004)
Sevoflurane depolarizes pre-synaptic mitochondria in the central nervous system
Acta Anaesthesiol Scand, 48 (5), 562-8
PubMed 15101849