HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



volume decrease (48). However, such evidence ap- 

 plies only to the steady part of the exercise; more 

 difficult to ascertain is the pattern of change in the 

 pulmonary blood volume from the start to the finish 

 of the exercise. In this regard, the most convincing clue 

 is the characteristic sequence of changes in the pulmo- 

 nary arterial pressure (fig. 28); this pattern is con- 

 sistent with an abrupt increase in the pulmonary blood 

 volume at the start of the supine exercise, a gradual 

 stabilization at below-peak values as exercise is con- 

 tinued, and a prompt fall to below resting values 

 when exercise is arrested (iog, 132). How the in- 

 creased blood volume is apportioned among the 

 different vascular segments of the lung is unknown; 

 however, the pulmonary capillaries apparently share 

 in the increase (364). 



Pulmonary Vascular Resistance 



The calculated pulmonary vascular resistance either 

 remains unaltered (iog) or, more often, decreases 

 (101, 346) during light to moderate (supine) exercise. 

 Although it is generally believed that the decrease in 

 calculated resistance at these levels of exercise repre- 

 sents both the widening of patent pulmonary vessels 

 and the opening of closed vessels (208, 241, 346), the 

 particular mechanisms which are responsible for this 

 change in vascular geometry remain speculative. 

 Three reasonable alternatives come to mind : active 

 pulmonary vasodilatation, passive dilatation by the 

 decrease in pleural pressure, or passive dilatation by 

 the increase in luminal pulmonary arterial blood 

 pressure. Of the three alternatives, the passive increase 

 in pulmonary arterial luminal (and transmural) pres- 

 sure seems sufficient — without invoking vasomotric- 

 ity — to account for the widening and opening of the 

 pulmonary vessels at these low grades of exercise (187). 



During heavy exercise, as the pulmonary blood 

 flow is more than tripled, the pulmonary vascular 

 resistance (calculated on the basis of an assumed left 

 atrial pressure) is described as becoming constant 

 (252). As pointed out previously, the pulmonary 

 vascular tree is then pictured as behaving as though it 

 were comprised of "rigid tubes"; the "rigid tubes," 

 in turn, are envisaged as wide-open, low-resistance 

 vessels with elastic fibers stretched to tighten their 

 collagen "jackets" (187). Generally speaking, the 

 calculations of pulmonary vascular resistance during 

 heavy exercise on the basis of pulmonary arterial 

 pressure and flow (fig. 34) are consistent with this 

 view. However, this interpretation of calculated 

 resistance is handicapped by the lack of assurance 



concerning the simultaneous behavior of the left 

 atrial pressure, the pulmonary blood volume and the 

 pleural pressures. Indeed, without information about 

 these critical parameters, the ratio of pulmonary 

 arterial pressure to pulmonary blood flow during 

 heavy exercise may represent either an increase or a 

 decrease in pulmonary vascular resistance. Finally, as 

 indicated previously, not only may the kinetic energv 

 in the pulmonary artery exceed the potential energy 

 at high rates of pulmonary blood flow, but intercon- 

 versions of potential and kinetic energy are bound to 

 occur along the length of the pulmonary vascular tree 

 (20). Consequently, during heavy exercise, even the 

 ratio of the pulmonary vascular pressure gradient 

 (potential energy gradient) to the pulmonarv blood 

 flow need not provide a reliable index of pulmonary 

 vascular dimensions. 



MISCELLANEOUS MECHANICAL INFLITENCES 



Heart Rate 



In normal dog and man, speeding up of the heart 

 rate by atropine, is ordinarily without appreciable 

 effect on pulmonary vascular blood pressures or blood 

 flow (424); in some instances the cardiac output may 

 increase by 40 to 50 per cent (168). In patients with 

 "tight" mitral stenosis, even the slight increment in 

 cardiac output induced by atropine may suffice to 

 precipitate pulmonary edema by elevating pulmonary 

 venous and pulmonary capillary pressures. 



Slowing of the heart has been produced by vagal 

 stimulation in dogs: as the heart rate drops to one- 

 half or one-third of the initial value, the cardiac out- 

 put falls and the pulmonary venous pressure rises 

 (65). A similar combination of bradycardia, low 

 cardiac output, and high pulmonary venous pressure 

 also occurs when intracranial pressure is considerably 

 increased; in this case, the occurrence of pulmonary 

 edema is often potentiated by left ventricular failure 

 from intense systemic vasoconstriction. Measures 

 which prevent the bradycardia or left ventricular 

 overwork also protect against the pulmonary edema 

 of increased intracranial pressure (65). 



"Bronclwmotor Tone" 



This colloquialism refers to a state of partial con- 

 traction of bronchial smooth muscle (95, 132, 351). 

 An increase in "bronchomotor tone" may conceivably 

 affect pulmonary vascular dimensions in at least three 



