1. Influence of anaesthesia and analgesia on the control of breathing
A Dahan, L.J. Teppema 
British Journal of Anaesthesia 
Volume 91, Issue 1, Pages (July 2003)
DOI: /bja/aeg150
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

2. Fig 1
The effect of placebo and antioxidant pretreatment on halothane-induced depression of the ventilatory response to acute isocapnic hypoxia in humans. Values are mean (sem) (n=8 subjects per treatment level). Halothane concentration was 0.11 end-tidal volume percent. Antioxidants are effectively able to prevent any depressant effect from low-dose halothane on the carotid bodies. Data are from Teppema and colleagues.14
British Journal of Anaesthesia  , 40-49DOI: ( /bja/aeg150)
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

3. Fig 2
The relationship between ascorbic acid production and depression of the ventilatory response to hypoxia by 0.5 end-tidal percent halothane. Note that humans have lost their ability to produce the antioxidant and have the greatest depression of the hypoxic response by halothane.
British Journal of Anaesthesia  , 40-49DOI: ( /bja/aeg150)
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

4. Fig 3
The relationship between metabolism and depression of the acute hypoxic response at 0.1 MAC anaesthetic concentration in humans.
British Journal of Anaesthesia  , 40-49DOI: ( /bja/aeg150)
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

5. Fig 4
Possible dose–effect relationships as given by the equation Ec=E0(1–cb) for three values of b. When b=1, the response curve becomes linear. Note that the model allows the effects of 0 and <0 to occur. E0=pre-drug effect, C50 is the concentration causing 50% effect or 0.5E0.
British Journal of Anaesthesia  , 40-49DOI: ( /bja/aeg150)
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

6. Fig 5
Response surface modelling of the interaction of remifentanil and propofol on resting ventilation (left) and resting PE′CO2 (right). Note the difference in scale direction of the x- and y-axes for the left and right graphs. Left: baseline ventilation (i.e. before any agent was given) is 9 litres min−1. The C50 values for remifentanil and propofol are 3 ng ml−1 and 16 µg ml−1, respectively. The interaction has a marked synergistic nature (INT=2). Right: baseline PE′CO2 (i.e. before any agent was given) is 5.5 kPa. The C50 values for remifentanil and propofol are 6 ng ml−1 and 37 µg ml−1, respectively. The interaction has a synergistic nature (INT=1.3). The high C50 values for propofol are the result of the slow propofol infusion allowing ample time for build-up of carbon dioxide in the body – despite the decrease in metabolism due to propofol – and consequently the central stimulation of breathing. Data are from Nieuwenhuijs.45
British Journal of Anaesthesia  , 40-49DOI: ( /bja/aeg150)
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

7. Fig 6
Response surface of the interaction of remifentanil and propofol on the ventilatory response to carbon dioxide. Baseline value (i.e. before any agent was given) was 1.9 litre min−1 per mm Hg. The C50 values for remifentanil and propofol are 8.6 ng ml−1 and 1.0 µg ml−1, respectively. The interaction has a synergistic nature, INT=1.3. The difference in C50 values between resting ventilation (5, left) and ventilation at various fixed PE′CO2 levels (this figure) occurs because carbon dioxide dynamics and kinetics were not taken into account when modelling resting ventilation (after drug infusion carbon dioxide will accumulate and affect resting ventilation under closed-loop conditions), while carbon dioxide dynamics has been eliminated when studying ventilation at various or just one fixed PE′CO2 level(s). Data are from Nieuwenhuijs.45
British Journal of Anaesthesia  , 40-49DOI: ( /bja/aeg150)
Copyright © 2003 British Journal of Anaesthesia Terms and Conditions