DYNAMICS OF PULMONARY CIRCULATION 



'7'7 



different ways: /) by mechanical distortion of the 

 pulmonary arterial tree and of the large pulmonary 

 veins which lie adjacent to the tracheobronchial tree; 

 2) by raising intra-alveolar pressure to compress the 

 pulmonarv capillaries and to increase, thereby, their 

 resistance to perfusion; and j) by increasing the 

 "elastance" of the lung (ig, 305, 351 ), i.e., the elastic 

 forces which are developed during each respiratory 

 cycle. Many experimental (95, 305) and clinical 

 observations attest to the capacity of the bronchial 

 smooth muscle to undergo drastic changes in tone in 

 response to appropriate stimulation; this severe type 

 of bronchospasm poses no problem in recognition. 

 More troublesome is the prospect that subtle changes 

 in "bronchomotor tone" mav escape detection (351). 

 As a general approach, bronchomotor tone may 

 reasonably be considered to remain unchanged during 

 the course of an experiment if: a) clinical evidences of 

 bronchial obstruction or dyspnea do not appear; b) 

 the ventilatory pattern remains unchanged; and c) 

 the mechanical properties of the lungs remain un- 

 altered (132, 153). When the nature of the experiment 

 precludes such clinical and experimental stability, 

 decision as to the influence of altered bronchomotor 

 tone on pulmonary hemodynamics falls to the experi- 

 menter. 



Following complete collapse, only 10 to 15 per cent 

 of the cardiac output perfuses the collapsed lung (316). 



Several different ways have been used to trace the 

 sequential changes in perfusion following bronchial 

 obstruction : the change in peripheral arterial oxygen- 

 ation (316), the change in "venous admixture'" (23) 

 and angiography (85). Although not entirely con- 

 sistent (5), the results seem to indicate that within an 

 hour after the bronchial obstruction, the blood flow 

 to the nonventilating lung is apt to decrease by 30 to 40 

 per cent (316). In time, the blood flow to the non- 

 ventilating lung decreases further; up to a month may 

 be required for nearly all mixed venous blood to be 

 excluded from the atelectatic lung and for systemic 

 arterial oxygenation to return toward normal values 

 (85). By way of contrast, the spontaneous restoration 

 of systemic arterial oxygenation in patients with 

 pneumonia or pneumothorax is more often a matter 

 of days than of weeks. 



The observation has been made that the pulmonarv 

 collateral circulation may proliferate in atelectatic 

 areas. However, the strong possibility exists that 

 complications of atelectasis, such as pulmonary infec- 

 tion, rather than the mechanical collapse, per se, are 

 responsible for the expanded collateral circulation 

 (316). 



Mechanical Compression (Atelectasis) 



It is well known that mechanical factors influence 

 the caliber of the pulmonary blood vessels and their 

 resistance to blood flow. For example, at a given 

 hydrostatic pressure head, moderately inflated lungs 

 contain more blood (wider vascular calibers) than do 

 either collapsed or markedly distended lungs (146); 

 similarly, pneumothorax not only decreases the air 

 content of the lungs but also shrinks the vascular 

 calibers (380). 



Atelectasis is generally believed to affect the pulmo- 

 nary circulation by mechanical compression. It has 

 been produced experimentally by bronchial obstruc- 

 tion (85, 94), pneumothorax (380) and sustained 

 hypoventilation (359). The changes following bron- 

 chial obstruction have been most intensively studied: 

 following complete occlusion of a bronchus, gas is 

 absorbed at a rate set by the composition of the gas, 

 the surface area and the rate of perfusion of the af- 

 fected area (94). As the gas content of the lung de- 

 creases, the mechanical compression of the pulmo- 

 nary blood vessels — particularly of the capillaries in 

 the collapsed alveoli — diverts the blood flow from the 

 atelectatic to the unaffected parts of the lung (85, 380). 



Hypertonic Solutions 



A particularly puzzling phenomenon has been the 

 occurrence of pulmonary arterial hypertension fol- 

 lowing the injection of hyperosmotic solutions, e.g., 

 20 per cent sodium chloride, into a peripheral vein 

 (28). Different mechanisms have been proposed to 

 account for this pressor response, including selective 

 constriction of the superior pulmonary veins at their 

 entry into the left atrium (120). Recently, microscopic 

 examination has shown that intravascular red-cell 

 agglutination occurs after the injection of highly con- 

 centrated salt and sugar solutions, raising the possi- 

 bility that luminal obstruction, rather than vasocon- 

 striction, may underlie the pulmonary pressor response 

 to hypertonic solutions (333, 376). 



PULMONARY VASOMOTOR ACTIVITY 



It has been shown in a previous section that the 

 pulmonary circulation is equipped with vascular 

 smooth muscle and nerves, and that the pulmonarv 

 circulation has the ability to vasoconstrict and to 

 vasodilate. Much more difficult to decide is whether 



