Background: Volatile anesthetic agents have been shown to have contractile
effects in vascular tissues during specific conditions. This study compared
contractile effects of halothane and sevoflurane in rat aorta treated with
verapamil, This study also tried to elucidate the mechanism of the contrac
tion.
Methods: Endothelium-denuded rat thoracic aorta was used for recording of i
sometric tension and measurement of influx of Ca-45(2+). All experiments we
re performed in the presence of verapamil, In recording of tension, rings w
ere precontracted with a submaximum dose of phenylephrine, followed by expo
sure to halothane or sevoflurane. For measurement of influx of C-45(2+), ra
t aortic strips were exposed to phenylephrine and then to additional haloth
ane or sevoflurane. Influx of Ca2+ was estimated by incubating the strips i
n Ca-45(2+)-labeled solution for 2 min.
Results: Halothane (0.5-4.0%) induced contraction in a dose-dependent manne
r, whereas sevoflurane (1-4%) had no effect on tension. Influx of Ca-45(2+)
was strongly enhanced by halothane at 1% and 2%, but only slightly at 4%,
and was not affected by 1-4% sevoflurane, SK&F 96365, a blocker of voltage-
independent Ca2+ channels, abolished contraction and influx of Ca-45(2+) by
1% halothane, Depletion of Ca2+ from the sarcoplasmic reticulum with ryano
dine or thapsigargin reduced the contraction induced by halothane at 4% but
not that at 1% and 2%.
Conclusion: Halothane is suggested to cause contraction by enhancing influx
of Ca2+ tin voltage-independent Ca2+ channels at concentrations up to 2% a
nd by inducing release of Ca2+ at 4%. Sevoflurane (1-4%) is devoid of these
contractile effects.