A Three Phase Theory About the Basic Respiratory Pattern Generator
It is generally accepted that the neurones which generate rhythmic respiratory activity are located in the lower brainstem and that these neurones are not dependent for their rhythmicity on phasic sensory inputs. Until recent years the rhythmicity of respiration was widely held to be the result of antagonistic connections between two populations of inspiratory and expiratory bulbar neurones. Although antagonistic inhibition has been demonstrated between these neurones (Mitchell and Herbert 1974, Richter et al. 1979) the significance of such inhibition for rhythmicity remains doubtful since in eupnoeic breathing expiratory intercostal and abdominal muscles are usually not active and expiration is ‘passive’, i.e., bulbar expiratory activity may not be essential to the maintenance of a normal inspiratory rhythm. One approach then to the problem of central rhythmicity would be to concentrate on the mechanisms generating the inspiratory rhythm. However, an equally important aspect of this problem concerns the nature of the central mechanisms, which enable controlled ‘passive’ expiration to occur, and how they are distinguished from mechanisms producing ‘active’ expiration. These mechanisms can all be defined with reference to events occurring in bulbar inspiratory neurones. Thus, what are the mechanisms which are responsible for: (1) Terminating the ramp-like activity of inspiratory neurones, i.e., what is the mechanism of the inspiratory ‘off-switch’ (von Euler et al. 1973)? (2) Relaxing inspiratory muscle tone after the inspiratory phase of the ventilatory cycle has come to an end, i.e., is there a central control of “passive” expiration? (3) Delaying re-activation of the inspiratory ramp, i.e., is there an inspiratory ‘gate’?
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