RESISTANCE AND CAPACITANCE PHENOMENA IN VASCULAR BEDS 



94' 



varying from around 2 with pure plasma to around 5 

 at high hematocrit readings when measured in a low 

 velocity viscosimeter (fig. 6). Lower relative viscosities 

 are obtained with high velocity viscosimeters and 

 still lower relative viscosities are noted in perfused 

 organs. The relative viscosity in the latter two systems 

 decreases as the pressure difference and flow rate are 

 raised. Most of the viscosity of normal blood is due 

 to the suspended red cells, but the effect of the cells 

 is slight until the hematocrit begins to exceed 30 

 per cent (40, 74, 115); however, the plasma proteins, 

 particularly the globulins, contribute significantly 

 (112). In terms of effective oxygen delivery to the 

 tissues, a hematocrit of around 45 appears to represent 

 the best compromise between viscosity and O2 

 carrying capacity (50). 



Effects of Extravascular Pressure on 

 Pressure-Flow Relationships 



In most vascular beds extravascular pressure 

 exerts little effect. However, in muscle vascular beds, 

 a marked increase in resistance to flow occurs with 

 contraction. This is exemplified best in the myo- 

 cardium in which during svstole a rise in resistance 



FLOW 



PERIPHERAL PRESSURE 



fig. 7. Records of systemic arterial pressure (BP), and 

 lateral pressure (CP) and moment-to-moment flow (F) in 

 the descending ramus of the left coronary artery during the 

 period labeled "flow." During the period labeled "peripheral 

 pressure" flow was interrupted by occlusion of the coronary 

 artery inflow proximal to the site of pressure measurement so 

 that the gauge recorded "peripheral coronary artery pressure." 

 Note that the latter pressure begins to rise during the phase of 

 isometric contraction that precedes the rise of systemic arterial 

 pressure, and that the peripheral coronary pressure begins to 

 fall with the onset of protodiastole, just before the incisura in 

 the systemic arterial pressure. [Reproduced in modified form 

 from Denison & Green (19).] 



occurs which closely parallels intraventricular pres- 

 sure in magnitude and duration, as shown in figure 7 



(19. 43 >• 



Coles & Gough (10) applied external pressure to a 

 cup applied to a digit while observing the capillaries 

 with a microscope. They noted that arrest of capillary 

 flow occurred consistently at cup pressures of 32 to 

 60 mm Hg in subjects with mean brachial artery 

 pressures of 80 to 1 20 mm Hg obtained with the 

 sphygmomanometer. They spoke of the pressure at 

 which flow ceased as the critical closing pressure and 

 reported that it rose with the arterial pressure in 

 hypertensives and fell with digital vasodilation 

 induced by body warming. The use of the term 

 "critical closing pressure" in this sense seems to us to 

 be ambiguous. Quite possibly, in their experiments 

 the pressure decreased progressively from the brachial 

 artery to the small digital arteries. If this were the 

 case the vessels in the digits may have collapsed when 

 the extravascular pressure just exceeded the intra- 

 vascular pressure. However, since the true intra- 

 luminal pressure of the vessels which close was 

 unknown, the role of the elastic forces producing 

 critical closure (see Burton, Chapter 6, vol. 1, sect. 2, 

 of this Handbook) as against the role of simple mechani- 

 cal collapse can hardly be differentiated. This makes 

 it quite difficult to assign a figure for the critical 

 closing pressure if indeed one may use that concept 

 here. 



Cerebrospinal fluid pressure may have a tendency 

 to vary directly with cerebral blood flow; however, 

 artificially induced changes of cerebrospinal fluid 

 pressure have little effect on flow unless the pressure 

 is elevated above arterial pressure (76 and un- 

 published data). 



Effects of Alteration of Venous Pressure 



When extremities were perfused with varying 

 pressures, while venous pressure was altered simul- 

 taneously so as to maintain artery to vein pressure 

 difference constant, flow still varied with the level of 

 the arterial pressure (89). The authors conclude that 

 some vascular structures were dilated as the arterial 

 (and total) pressure throughout the vascular bed 

 rose. In the supine anesthetized dog, inspiration was 

 accompanied by a rise of intra-abdominal pressure 

 and of small vein pressure in the hind leg. Widely 

 opening the abdomen abolished both (113). The 

 small vein pressure effects apparently were trans- 

 mitted peripherally from the inferior vena cava. 



