PH\SICAL EQUILIBRIA OF HEART AND VESSELS 



103 



method" to o\ercumc tliis cliBiculty (9). It suffers 

 from the usual Hmitations of any method which 

 depends upon a "lumped parameter" theory. In 

 this instance the assumption is made that the actual 

 resistance to flow of a vascular bed can be considered 

 as if it were the resistance of a "single equivalent 

 vessel" representing the actual distributed resistance 

 and distributed distensibility of the whole bed. With 

 respect to the resistance, this assumption is not too 

 far from validity, since so much of the total re- 

 sistance, particularly with vasomotor tone, resides 

 in the arterioles. 



The principle of the method is that if, after the 

 active tension has increased producing a decrease 

 in radius (and increase in resistance), the resistance 

 vessels were brought back to their original size, then 

 the elastic tension would be the original elastic 

 tension. The increase in total tension would then 

 be entirely due to this increase in active tension, 



T = Ta + Te = T,, + f(r) 

 and if r is unchanged, 



\T = ST^ = 



APt 



(24) 



(25) 



The method ot constant flow perfusion was used 

 for an isolated rabbit's ear. When pressor agents, 

 e.g., adrenaline, were added to the perfusate, the 

 vasoconstriction showed itself by increase in driving 

 pressure (measured by the pressure at the arterial 

 cannula). 



An increase in transmural pressure of the \essel 

 was then produced by lowering the tissue pressure. 

 The ear was in a box, in which pressures less than 

 atmospheric could be produced. With sufficient 

 negative pressure, the driving pressure could be 

 reduced to the original \alue that had been recorded 

 before the vasoconstriction had occurred. At this 

 "null point," both flow and driving pressure were 

 at their original values, so the resistance and the 

 radius of an "equivalent single vessel" would also 

 be at their original values. In this circumstance, the 

 change in active tension that had occurred would 

 be proportional to the change in Ptv, i.e., to the 

 negative tissue pressure that had been required to 

 reach the null point, i.e.. 



r.4 = — r X APt- (r constant) 



(26) 



It would be quite impractical to use such a null 

 method routinely to measure active tension, for the 

 large negative tissue pressure very soon causes edema 



of the tissues of the ear, and leakage from distended 

 venous vessels. However, the method could be used 

 to find whether any of the more commonly used 

 methods of measuring the effect of pressor drugs on 

 vascular beds might give a linear relation to the 

 active tension. There are three ways one can make 

 resistance measurements on vascular beds. 



a) At constant pressure of perfusion, measuring 

 the reduction in flow when vasoconstriction occurs. 

 The results can be expressed as an increase in vascular 

 resistance. 



h) At constant flow, as provided by a positive 

 perfusion pump, measuring the rise of dri\ing pressure 

 that occurs when vasoconstriction occurs. Again 

 the results can be expressed as an increase of re- 

 sistance. 



c) As in the intact animal, where neither driving 

 pressure nor flow is kept constant, though often the 

 pressure is not altered so much as the flow. Here 

 changes in both pressure and flow must be meas- 

 ured, and the change in resistance calculated. 



240 



210 



E 180 



t 150 



3 120 



90 



60 



30- 



20 



ADnving pressure (mm Hg) 

 J 1 I I I I I I I L. 



30 



60 



J I I 



90 



120 



150 



FIG. 20. Linear relation between the active tension in 

 vascular smooth muscle, as estimated by the null method, and 

 the rise in arterial pressure at constant flow. Data for 10 diff'er- 

 ent rabbit ears are included; for individual ears the correla- 

 tion was much higher. [From Burton & Stinson (28).] 



