1. Effects of sevoflurane on sympathetic neurotransmission in human omental arteries and veins 
K Thorlacius, C Zhoujun, M Bodelsson 
British Journal of Anaesthesia 
Volume 90, Issue 6, Pages (June 2003)
DOI: /bja/aeg135
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

2. Fig 1
Frequency–response curves obtained by electrical field stimulation (EFS) of human omental artery (a) and vein (b) segments in the presence of sevoflurane 0, 1%, 2% or 4%. In both artery and vein segments, sevoflurane 4% attenuated EFS-induced contractions compared with control. *P<0.05, two-way repeated-measures anova followed by Dunnett's post hoc test. Values are expressed as percentage of the reference contractions, which for arteries were mean 2.2 (sd 1.8) mN (n=9), 2.7 (1.8) mN (n=6), 2.4 (1.8) (n=7) mN and 3.6 (2.7) mN (n=7), respectively, and for veins were 11.7 (9.2) mN (n=8), 10.5 (9.4) mN (n=7), 10.5 (4.7) mN (n=7) and 17.4 (10.3) mN (n=7), respectively.
British Journal of Anaesthesia  , DOI: ( /bja/aeg135)
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

3. Fig 2
Concentration–response curves obtained with exogenous norepinephrine (NE) in human omental artery (a) and vein (b) segments in the presence of sevoflurane 0, 1%, 2% or 4%. In the artery, but not the vein segments, sevoflurane 4% attenuated the NE-induced contractions compared with control. *P<0.05, two-way repeated-measures anova followed by Dunnett's post hoc test. Values are expressed as percentage of the reference contractions, which for arteries were: mean 25.3 (sd 7.7) mN, 25.2 (12.4) mN, 28.9 (13.4) mN and 24.1 (9.3) mN, respectively, and for veins 14.9 (3.7) mN, 13.4 (4.0) mN, 13.6 (3.3) mN and 12.5 (4.0), respectively (all n=6).
British Journal of Anaesthesia  , DOI: ( /bja/aeg135)
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

4. Fig 3
Release of [3H]-NE induced by electrical field stimulation (EFS) from human omental artery (a) and vein (b) segments pre-incubated with [3H]-NE. EFS was applied in the presence of sevoflurane 0, 1%, 2% or 4%. NE release was reduced in arteries in the presence of sevoflurane 2% and 4% and veins in the presence of sevoflurane 1%, 2% and 4%, respectively, compared with control. *P<0.05, two-way repeated-measures anova. Values are expressed as percentage of the initial reference release (at 32 Hz) which for arteries were: mean 0.85 (sd 0.78) pmol (n=12), 0.56 (0.75) pmol (n=7), 0.70 (0.92) pmol (n=8) and 0.60 (0.71) pmol (n=9), respectively, and for veins were: 0.55 (0.62) pmol (n=13), 0.34 (0.19) pmol (n=6), 0.34 (0.16) pmol (n=6) and 0.48 (0.54) pmol (n=6), respectively.
British Journal of Anaesthesia  , DOI: ( /bja/aeg135)
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

5. Fig 4
Uptake of tritium into human omental artery (filled bars) and vein (open bars) segments incubated with [3H]-NE in the presence of 0 (control) or sevoflurane 1%, 2% or 4% or in the presence of desipramine. Desipramine reduced uptake in the artery and vein segments. Sevoflurane did not affect uptake. *P<0.05, one-way repeated-measures anova followed by Dunnett's post hoc test. Values are mean (sd); n=7 and 6 for arteries and veins, respectively.
British Journal of Anaesthesia  , DOI: ( /bja/aeg135)
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions