Spinal Cord is the Primary Site of Action for Skeletal Muscle Relaxation by Sevoflurane.

Abstract

A randomized, in vivo study was performed to explore the skeletal muscle relaxation action site of sevoflurane. The aim of this study was to investigate the skeletal muscle relaxation action of sevoflurane by a modified selective anesthetics delivery rabbit model. The action site and mechanisms of skeletal muscle relaxation caused by sevoflurane were unclear, so a modified selective anesthetics delivery model was used. Sixteen male New Zealand White rabbits were randomly assigned to the sevoflurane or sham group. In situ measurement of train of four, maximum single twitch, and tetanic muscle force of left tibialis anterior muscle was repeatedly measured at three time points: at the beginning of lower torso bypass (baseline value), during preferential sevoflurane delivery to the brain (brain value), during preferential sevoflurane delivery to the spinal cord (spinal cord value). When 1.5MAC sevoflurane was administrated via the lungs, the arterial concentration and partial pressure of sevoflurane in the upper torso were 205.27 ± 16.23 μg/mL and 29.16 ± 1.05 mmHg, whereas in the lower torso bypass circulation were 10.39 ± 4.50 μg/mL and 1.79 ± 0.97 mmHg. Conversely, the arterial concentration and partial pressure of sevoflurane in the upper torso were 14.04 ± 5.33 μg/mL and 2.25 ± 0.84 mmHg, whereas those values were 199.38 ± 11.61 μg/mLl and 29.20 ± 1.08 mmHg in the lower torso, when 1.5MAC sevoflurane was delivered via an oxygenator. In sevoflurane group, maximum single twitch and tetanic muscle force were significantly reduced compared with baseline (single: P = 0.046; tetanic: P = 0.001) or brain values (single: P = 0.005; tetanic: P = 0.001), when spinal cord was selectively anesthetized. In the sham group, there were no significant differences among the three conditions compared. A modified selective anesthetics delivery rabbit model has been validated, which provided evidence that the spinal cord, not the brain, was the primary site mediating the skeletal muscle relaxation action of sevoflurane. 5.