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The increase in airway resistance that follows the breathing of fine inert dust was first demonstrated by DuBois and Dautrebande (1), who also showed that an aerosol of carbachol had the same effect. The compliance of the lungs was reduced, which led these authors to conclude that the increased airway resistance was unevenly distributed. Constantine and associates (2) confirmed the increased airway resistance in similar experiments and also noted an increase in intrathoracic gas volume, which they attributed to trapping of gas. McDermott (3) found a significant increase in airway resistance after breathing similar dusts at concentrations almost certainly less than those used by the previous workers and more comparable to the concentrations encountered under certain industrial conditions. She also commented on the considerable individual variation in response. The first part of the present study had two main objectives, the first of which was to determine the extent to which these inhaled materials altered the distribution of alveolar ventilation and to observe the effects this had upon respiratory gas exchange in the lungs. Of at least equal importance was the possibility that the experiments might reveal something of how the distribution of alveolar perfu-sion responds to an acute alteration in the distribution of alveolar ventilation, and this has influenced the design of the experiments. During these experiments the possibility arose that the observed effects might result from the associated moderate hyperventilation. A preliminary observation lent support to the idea that hy-perventilation was followed by an increase in * physiological dead space, and this led to the second series of experiments. The results, which have already been reported briefly (4), showed a prolonged increase in physiological dead space after hyperventilation in the sitting position. This was prevented by substituting a mixture containing carbon dioxide for air during the period of hyperventilation and was much less evident when the subjects were supine. Methods Respiratory gas exchange was investigated by the measurement of the alveolar-arterial difference in oxygen tension (A-aD) and physiological dead space. Expired gas was collected in a Tissot spirometer for 2 minutes and was analyzed by the Scholander method. During this time three samples of blood for estimation of Po2 and two samples for Pco2 were obtained from a needle in the brachial artery, sampling extending over the whole of the 2-minute period. The Po2 of arterial blood was measured within 10 minutes of sampling by a polythene-covered combined electrode …

journal of clinical investigation

Alterations in Ventilation-Perfusion Relationships in the Lung after Breathing Inert Dust or Bronchoconstrictor Aerosols and after Short Periods of Voluntary Hyperventilation