Relative dimensions of bronchioles and parenchymal spaces in lungs from normal subjects and emphysematous patients

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      As a part of a continuing program of study of the morphology of lungs from emphysematous and aging subjects, tissue samples containing the “smallest” non-respiratory bronchiole from twelve emphysematous patients and twelve normal subjects were subjected to planimetry. The mean cross sectional area of various structures in the two groups were statistically compared.
      The most striking aspect of the study was a marked restriction of the mean area of the lumens of non-respiratory bronchioles in pulmonary emphysema. Since there was no demonstrable relationship between age and lumen size in either group, bronchiolar stenosis was considered to be an inherent characteristic of lungs from emphysematous patients. There was also a much smaller mean number of alveolar attachments per bronchiole in patients with emphysema than in the control group. This association of bronchiolar stenosis and reduced alveolar attachments is in accordance with the view that the stenosis is largely due to loss of alveolar radial support with resulting collapse of the semi-rigid tubules. On the other hand, the mean areas of bronchiolar mural tissue and epithelium were comparable in both groups, so that the stenosis of bronchioles did not seem to be primarily a function of increased bulk of their walls or linings. Hypertrophy and spasm of bronchiolar smooth muscle and intraluminal exudates could not be measured but were considered plausible explanations for clinically reversible airway obstruction.
      The individual distal air spaces quickly lost their identity in emphysema due to the processes of overexpansion and disruption of the parenchymal tissue. It was therefore necessary to classify all alveoli and alveolated structures simply as parenchymal spaces. Parenchymal spaces in emphysematous patients were of larger mean size and fewer in number than in the normal control subjects. Moreover, there was extreme variability in their individual sizes. The greater mean size was due to the presence of a relatively few number of extremely large dilated openings. It was of interest that there was also a greater number of the smaller space sizes in emphysema. This, apparently, was due to “crowding” and compression by the large defects.
      Since there were similar mean amounts of parenchymal tissue in the samples from emphysematous and normal subjects, it was reasoned that the individual parenchymal spaces, in general, must have thicker walls. This was interpreted as an effect of interstitial alveolar inflammation and fibrosis which we have previously observed to be quite common in emphysema.
      There was no demonstrable relationship between emphysema and alterations in blood vessels.
      All of these findings were considered to be consistent with our earlier stated views on the pathogenesis of pulmonary emphysema. Thus the pulmonary parenchyma may be either ruptured or weakened by recurrent bronchopulmonary inflammation. In such circumstances they are presumed to be more vulnerable to the stressful effects of abnormal, and possibly even normal, mechanical forces. Primarily due to loss of parenchymal tractional support, small bronchioles undergo varying degrees of collapse. Since these are the smallest air passages in the lungs, they are logically the points of greatest flow resistance. Abnormal mechanical pressures may result from distention within distal air spaces by air trapping behind stenotic bronchioles. It may also occur as a result of external tension from fibrous contracture of inflamed adjacent parenchyma. Atelectasis, resection of a portion of the lung and change in the shape of the chest may have a similar effect.
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