The purpose of this study were to elucidate how sevoflurane affects vascular smooth muscle and to understand the intracellular mechanism of sevoflurane. Isolated aortic rings of the rabbit were examined. Rings were mounted on tissue bath
containing
40
ml of modified Krebs solution bubbled with 95% O2/5% CO2 and attached to force transducers. The preparations were contracted with either 40 mM KCI, or 0.1 ㎛norepinephrine followed by 0.1 ㎛acetylcholine (and 1 nM ryanodine)-or 2.8 mM lidocaine
induced
relaxation. At steady state contraction or relaxation, the effects of sevoflurane (2, 4, 5%) were studied. The steady state tension before administration of sevcflurane was considered as 100% and the changing tension during sevoflurane was
expressed as
a percentage. Sevoflurane (2, 4, 5%) produced relaxing effects (99.4±0.6, 98.1±0.9, 95.9±1.0%) on KCI-induced tension, tension, independent of endothelium. Sevoflurane increased tension in the acetylcholine (55.4±5.1%)- or lidocaine
(75.3±8.3%)-
relaxed state (acetylcholine: 73.6±5.3, 86.8±3.2, 94.1±5.2%, acetylcholine±ryanodine; 63.7±4.6, 68.6±7.2, 70.4±2.5%, lidocaine; 83.7±7.0, 84.6±12.1, 85.3±4.4%). The effects were dose-dependent manner.
It is concluded that sevoflurane directly alters vascular contraction or relaxation in relation to Ca2+ mobilization on condition and that mechanism of sevoflurane's effects on the sarcoplasmic reticulum may play a primary role.
|