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I was interested in the article by Burns and Gibson in the February issue of Thorax,1 but feel that the authors should exclude the following possible confounding factors which should be addressed before their hypothesis can be accepted.
The time course of the bronchoconstrictor response to deep breaths in mild asthma is brief (usually 60–90 seconds), so the precise timing of the sGaw measurements after the manoeuvre is critical. Have the authors taken this into consideration?
Although the pre-test and test breathing pattern was standardised as far as possible, have changes in Pco2 been excluded since hypocapnia can have a larger effect on sGaw even in normal subjects than that described here.2
Why do their normal subjects show a fall from baseline sGaw after deep breaths rather than the consistent small rise seen in previous studies as quoted in the discussion?
If these points can be answered, then further investigation of their inherently speculative hypothesis might indeed be worthwhile.
We agree with Dr Sterling that the bronchoconstrictor effect of a deep inspiration in asthma is brief and that the timing of the sGaw measurement is critical. The relevant comparison is between the sGaw performed after the timed non-forced inspiratory manoeuvres and that performed after the forced inspiratory manoeuvres. In each case, as stated in our paper,1 subjects returned to functional residual capacity (FRC) immediately after the final full inspiration, ensuring both parity in the timing of the two manoeuvres and that in each case sGaw was measured as soon as practically possible after the inspiration.
Pco2 was not measured but the inspiratory/expiratory manoeuvres preceding the measurement of sGaw were designed to be identical in their time-volume relationship. This was in order to minimise any difference in the behaviour of the smooth muscle (or any other element responsive to stretch), but it would, of course, also ensure that any difference in ventilation, and thus Pco2, was also minimised.
We compared sGaw after two different types of inspiratory manoeuvre which were designed to be identical in every respect other than the intrathoracic pressure generated. The constraints of this requirement meant that the inspiratory manoeuvres were different from the usual rapid deep inspiration preceding the measurement of sGaw in the referenced studies. The longer inspiratory manoeuvre in our study would be expected to produce a significantly diminished bronchodilating effect than that produced by the usual rapid deep inspiration.2 This probably explains the absence of any significant difference between the baseline sGaw (before deep inspiration) and that performed after deep inspiration (without resistance) in healthy subjects.
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