1. Desflurane but not sevoflurane can increase lung resistance via tachykinin pathways† 
J.-I. Satoh, M. Yamakage, T. Kobayashi, N. Tohse, H. Watanabe, A. Namiki 
British Journal of Anaesthesia 
Volume 102, Issue 5, Pages (May 2009)
DOI: /bja/aep041
Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

2. Fig 1
Anatomical basis of airway vagal nerve innervation and peripheral local regulation by these nerve reflexes. Ach, acetylcholine; VIP, vasoactive intestinal peptide; NO, nitric oxide; TKs, tachykinins (i.e. NKA, neurokinin B, substance P, calcitonin gene-related peptide); ASMs, airway smooth muscles; NP, neuropeptide. The vagal nerve supplies all parasympathetic, preganglionic neurones and the majority of sensory nerve fibres. Parasympathetic nerve stimulation can release acetylcholine, resulting in bronchoconstriction. Noxious stimuli such as tobacco smoking can activate sensory nerves (C-fibres) and release tachykinins antidromically via axonal reflexes. Tachykinins such as NKA cause bronchoconstriction, whereas other tachykinins induce airway inflammation.
British Journal of Anaesthesia  , DOI: ( /bja/aep041)
Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

3. Fig 2
Representative raw data of the effects of desflurane and sevoflurane on the respiratory parameters total lung resistance (RL) and dynamic lung compliance (CDyn). Exposure to a high concentration of desflurane (2.0 MAC=12.8% in guinea pigs) distinctly increased RL biphasically. In an inverse manner, the anaesthetic decreased CDyn biphasically. On the other hand, sevoflurane at the same potency (2.0 MAC=4.0% in guinea pigs) had little effect on RL, whereas the anaesthetic slightly but rapidly increased CDyn without showing the biphasic responses seen in the desflurane experiment.
British Journal of Anaesthesia  , DOI: ( /bja/aep041)
Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

4. Fig 3
Effects of desflurane and sevoflurane without any contractile agonists on changes in total lung resistance (RL) and dynamic lung compliance (CDyn). Data are expressed as mean (sd), n=6 each. *P<0.05, **P<0.01, vs each control value without exposure to an anaesthetic. The data are shown as the changes in the first and second peaks in the desflurane experiment, whereas the data in the sevoflurane experiment are shown as the maximal changes in the parameters because of its monophasic response. Desflurane significantly increased RL and decreased CDyn in a dose-dependent manner in both the first and the second peaks. However, sevoflurane had no effect on RL, whereas it slightly but significantly increased CDyn. There was no significant difference in the per cent change of RL between the first and the second peaks at 2.0 MAC desflurane.
British Journal of Anaesthesia  , DOI: ( /bja/aep041)
Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

5. Fig 4
Effects of 2.0 MAC desflurane on per cent changes in total lung resistance (RL) and dynamic lung compliance (CDyn) in the pretreatment of atropine 0.1 mg kg−1 and after vagotomy. Raw data for the vagotomy experiment is shown in the inset figure. Data are expressed as mean (sd), n=6 each. *P<0.05 vs baseline without exposure to an anaesthetic. †P<0.05 vs the other two groups. Although the contractile effects of desflurane on the respiratory parameters did not change by pretreatment with atropine, only the changes in the first peaks of the parameters RL and CDyn were partially inhibited by vagotomy, by ∼32% and 29%, respectively. The second peaks of the respiratory parameters did not change.
British Journal of Anaesthesia  , DOI: ( /bja/aep041)
Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

6. Fig 5
Effects of 2.0 MAC desflurane on per cent changes in total lung resistance (RL) and dynamic lung compliance (CDyn) in pretreatment with the tachykinin (TK) receptor NK1 and NK2 receptor selective antagonists, sendide (1 mg kg−1) and MEN (3 mg kg−1). Raw data for the TK antagonists experiment are shown in the inset figure. Data are expressed as mean (sd), n=6 each. *P<0.05 vs baseline without exposure to an anaesthetic. †P<0.05 vs the control values by exposure to desflurane. Because the first and second peaks of the respiratory parameters could not be distinguished in the treatment experiment, the per cent changes in these parameters at the same elapsed time as the control experiment were selected for the summarized data. Desflurane (2.0 MAC) had no effect on either RL or CDyn.
British Journal of Anaesthesia  , DOI: ( /bja/aep041)
Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

7. Fig 6
Effects of 2.0 MAC desflurane on per cent change in total lung resistance (RL) and dynamic lung compliance (CDyn) in the pretreatment with capsaicin (80 mg kg−1 total over three consecutive days). Raw data for capsaicin depletion experiment is shown in the inset figure. Data are expressed as mean (sd), n=6 each. *P<0.05 vs baseline without exposure to an anaesthetic. †P<0.05 vs the control values by exposure to desflurane. Because the first and second peaks of the respiratory parameters could not be distinguished in the treatment experiment, the per cent changes in these parameters at the same elapsed time as the control experiment were selected for the summarized data. Desflurane had no effect on RL, whereas it slightly but significantly increased CDyn, as was seen in the sevoflurane experiment using untreated animals.
British Journal of Anaesthesia  , DOI: ( /bja/aep041)
Copyright © 2009 British Journal of Anaesthesia Terms and Conditions