Macklin and Macklin 351 



the lung connective tissue, and so o\erlookecl what was not to him obvious; 

 (6) the lung was not fixed by intratracheal injection, but by immersion of small 

 blocks of tissue, and the air was squeezed out of these or diffused away in the 

 various technical manipulations. We feel that intratracheal fixation is very 

 important in the demonstration of air bubbles and the impressions made by 

 these in the pulmonic connective tissue. The lung, however, should not be 

 overdistended with fixative, for then the vascular sheaths arc dilated, giving 

 rise to an appearance simulating air in the sheaths.' Fisher's'" case, autopsied 

 within an hour or so after death, revealed the air in the mediastinum and 

 along the vessels very clearly. The case of Fisher and Macklin^' is another good 

 example of the value of prompt postmortem examination and intrabronchial 

 fixation. 



Interalveolar Po/rj.— Recent investigations in functional anatomy have 

 shown that interalveolar pores are an actuality.'""'' It has been suggested 

 that they allow air to diffuse into a region of lung whose bronchus has become 

 occluded and that thus they tend to prevent atelectasis. It may be that they 

 have some influence of this kind, but, if so, it is undeniable that atelectasis 

 occurs in spite of them. This may be, in small areas, because the pores have 

 become stopped up from the effect of inflammation; or in large areas because 

 the pores do not occur in the connective-tissue septa lying between secondary 

 lobules of lung substance. It is possible, too, that, when atelectasis does occur, 

 the consequent compensatory emphysema involves less alveolar overstrain 

 since, due to the free diffusion of air through the lung tissue on account of the 

 jiores, the area of alveolar ectasia is spread out more and so the alveoli in any 

 local area are not subjected to a breaking strain. Be that as it may, it is possible 

 that the presence of pores explains the freedom of some individuals from PIE 

 and its sequels when showing the leakage-predisposing conditions mentioned 

 in the paragraphs immediately preceding. We would certainly not say that 

 every person who develops these conditions will as a consequence have a PIE. 

 There is, however, no reason to think that pores are more abundant in the 

 lungs of some people than in others of the same age, so there seems to be no 

 sound explanation for immunity to PIE, if so it may be called, on the part of 

 a certain class of patient, on the basis purely of pore equipment. 



Hereditary Predisposition— On the other hand, it may be that susceptibility 

 to air leakage may rest, to some extent at least, on hereditary ground. This 

 applies not only to the cases already discussed, but to those which are to follow. 

 There may be an inherent weakness in the alveolar walls of some persons, 

 leading them to rupture more easily than normal, as evidenced by the numer- 

 ous records of recurrent pneumothorax'' and of familial pneumothorax.'^ 



Local Alveolar Overstrain.— Yrova these reports and many others that could 

 be cited, it appears reasonable to conclude that PIE is a concomitant of many 

 disease conditions and bronchial accidents that involve local alveolar over- 

 strain. We may affirm that any condition xvhich induces atelectasis inay pre- 

 cipilate compensatory overinflaiion, and this, in turn, particularly when aided 



