In artificially ventilated normal and diseased human lungs the distribution of resistances along the airways, between different parts of the lungs, and within emphysematous lesions has been measured and the percentages of elastic and non-elastic tissue and airway resistances calculated. Besides volume, flow, and pleural pressure within the respirator box up to three alveolar catheters, intrabronchial side and end pressure and tracheal catheters have been used to differentiate transpulmonary pressure into its components. Standard ventilation conditions for quiet breathing have been defined as FRC = 50 % TC (TC = V at p = 15 cm H₂O), breathing volume of about 10 % TC, and breathing frequency = 13-15/min which approximately equals in- and expiratory peak flow rates of about 0.2-0.3 1/sec/lung.Airway resistance was 1.57 (0.6-2.8) in normal and 18.43 (3.0-48.0) cm H₂O/l/sec/ lung in emphysematous lungs. Total resistance (Ppi-Pn·) could be differentiated into elastic resistance 72 %, airway resistance 16 %, and tissue resistance 12 %. In disease, particularly in bronchitis and emphysema, there was a marked change of these percentages with elastic resistance considerably lowered to a mean of 33 % and airway resistance increased to 38 %, in severe cases even up to 76 %. Tissue resistance was relatively high with mean values of about 40 % of non-elastic resistances.In normal lungs the directly measured alveolar pressures correspond at various sites, while in disease differences of regional alveolar pressures indicate inhomogeneity of resistances and ventilation. In emphysema three types of ‘closed’, ‘open’, and ‘half-open’ bullous lesions have been established. In half-open lesions the pressure levels lie between pleural and alveolar pressure of the surrounding lung tissue and thus may play a part in the formation of bullae. Moreover in emphysema the increase of airway resistance is caused mostly by the peripheral airways, but in some cases narrowing of the larger airways seems to play a part even in quiet or slightly reinforced breathing. In preparations of both lungs the resistance of the lower trachea limits flow, with the effect that the correction factor for airway resistance and dynamic compliance between one and both lungs is only 1.6 instead of 2.

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Pneumoconioses produced by intratracheal applications of various dusts (quartz, coal, cadmium and lead sulfide) in rats were investigated by electron microscopy in order to follow the pathway of the dust particles from the alveoli into the pulmonary interstitium.As postulated by Spencer in 1977 on the basis of light microscopic investigations, the dust particles produce necroses of the alveolar septae (‘alveolar ulcers’). Two forms of necroses appear to occur: with a less severe dust exposure, individual pneumocytes and their basement membrane are destroyed by dust particles. Dust-laden macrophages are deposited here which are displaced into the stroma after re-epithelization of the alveolar defect. On the other hand, with massive dust exposure, almost all pneumocytes of the affected alveoli become necrotic. The affected alveoli collapse and are replaced by connective tissue, so that the dust is situated in the connective tissue stroma.A transcellular penetration of the dust particles into the pulmonary interstitium or an immigration of dust-laden macrophages into the pulmonary stroma through the intercellular junctions of intact pneumocytes was not observed in any of the pneumoconiosis models.

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